Cocaine

After Lynley Graham’s custody photo was posted to a police force’s Facebook page, horrified users were quick to discuss the harmful effects of hard drugs

Deep lines etched across a woman’s face and cheeks sunken to the bone – this one shocking image illustrates the effects of substance abuse.

Lynley Graham’s custody picture has been released by Humberside Police after she was jailed for 18 months for drug offences.Graham was found in possession of class A drugs, including heroin and cocaine, and was subsequently charged with possessing a class A drug with intent to supply, Grimsby Live reports.

After the photo was posted to Humberside Police’s Facebook page on Wednesday, users were quick to discuss the 53-year-old’s weathered appearance.

Before and after pictures show a striking physical transformation.

One said: “I’m 64, I look young compared to her. Is she a lesson, perhaps, in what substance abuse can do to your skin?”

Another added: “Let’s hope some young people look at her and see what a life of drugs does apart from ruining entire families.”

Drug addiction and misuse contributed to more than 2,500 UK deaths in 2017.

Inhalants can cause damage to the kidneys, liver and bone marrow, and persistent drug consumption can result in abscesses, tooth decay – known as ‘meth mouth’ in the United States.

Other symptoms include premature ageing of the skin, often adding decades to someone’s appearance.

Rehabs.com, a US-based charity, has also published startling images of drug users to demonstrate the long-term toll narcotics have on one’s appearance.

Drugs can damage almost every system in the body; bloodshot eyes, dilated pupils, puffy faces and discoloured skin are all noticeable signs.

Some users suffer a rapid physical deterioration – with facial appearances sometimes ruined in just a matter of years.

Self-inflicted wounds, common among consumers of methamphetamine, can be caused by users picking at their skin to relieve the sensation of irritation – sometimes described as like crawling insects.

And a skeletal appearance can be the result of appetite-suppression.

Cocaine can commonly lead to chronic skin ulcers, pus-filled skin and the development of Buerger’s disease – an inflammation in small and medium-sized blood vessels.

Heroin has been known to dry the skin, leaving addicts with itchy and aged skin.

In May, Sir Angus Deaton, a world-leading economist, warned that drug abuse and alcoholism claim more lives of those in middle-age than heart disease.

‘Economic isolation’ is cited as one of the biggest contributors.

In 2017, a poll of 1,600 adults found that almost nine in ten said that seeing the physical effects of hard drugs made them less likely to take them.

The publication of such images is a common tactic among anti-addiction campaigners.

Scotland is experiencing its own drug crisis, with a 27 per cent rise in drug-related deaths, according to official statistics.

It puts Scotland’s drug mortality rate three times higher than the UK as a whole, and higher than any other country in the European Union.

Millions of Americans are trapped in a cycle of drug abuse and addiction: In 2013, over 24 million reported that they had abused illicit drugs or prescription medication in just the past month. More than 1.7 million were admitted to treatment programs for substance abuse in 2012. The pursuit of a drug habit can cost these people everything – their friends and family, their home and livelihood. And nowhere is that impact more evident than in the faces of addicts themselves.

Here, the catastrophic health effects of drug abuse are plain to see, ranging from skin scabs to decayed and missing teeth. While meth is often seen as one of the most visibly destructive drugs, leading to facial wasting and open sores,various other illicit drugs, and even prescription medications can cause equally severe symptoms when continuously abused. The use of opioids like OxyContin or heroin can cause flushing and a rash of red bumps all over the skin, while cocaine abuse can result in a significant drop in appetite and dangerous malnutrition and weight loss. Ecstasy may cause grinding of teeth, and smoking cannabis releases carcinogens and other chemicals that can diminish skin collagen and produce an appearance of premature aging. Even alcohol abuse can lead to wrinkles, redness, and loss of skin elasticity.

Beyond the direct effects of substance abuse, perhaps its most damaging result is addiction itself. The compulsion of addiction makes drug use the most important purpose in an addict’s life, leading them to pursue it at any cost and treat anything else as secondary. Self-neglect becomes normal – an accepted cost of continuing to use drugs. And the consequences of addiction can remain etched in their very skin for years.

Do FDA-approved psychostimulants increase the risk of cardiovascular events?

There is no convincing evidence that FDA-approved psychostimulants (e.g. methylphenidate, dextroamphetamine, amphetamine salts, and atomoxatine) increase the risk for cardiovascular events among patients without pre-existing cardiovascular disease (CVD). However, among those with pre-existing heart disease, including arrhythmias, coronary artery disease, heart failure, or in patients for whom an increase in heart rate or blood pressure could be harmful, psychostimulants may increase the risk for cardiovascular events.

How does cocaine end up as the number two cause of drug deaths, just behind opioids? Excluding adulteration with opioids, how does cocaine kill you?The effects of cocaine on the cardiovascular system can be grouped into acute and chronic processes. Cocaine use can cause one or more of several acute, life-threatening cardiovascular effects. The most common is myocardial ischemia or infarction (e.g. a heart attack). Cocaine can induce a heart attack through one of several mechanisms. First, cocaine causes arterial (including coronary artery) vasoconstriction, which can lead to coronary vasospasm. Second, cocaine activates platelets, which increases the risk of thrombosis (including coronary thrombosis). Third, cocaine use produces an adrenergic surge which induces tachycardia (high heart rate) and hypertension. High heart rate and hypertension both increase myocardial oxygen demand, which can cause supply-demand mismatch and precipitate myocardial ischemia or infarction. Fourth, vasospasm or stress associated with cocaine use can also precipitate coronary artery plaque rupture (the mechanism underlying most classic heart attacks).

Two thirds of heart attacks due to cocaine occur within three hours of cocaine use; the risk of a heart attack is 24-fold higher than normal in the first sixty minutes after using cocaine. Cocaine has several other potentially devastating acute effects, including stroke, aortic dissection (e.g. dissection of the major artery connecting the heart to the rest of the body), life threatening heart arrhythmias, and myocarditis which can also occur with chronic use. Chronic cocaine can result in accelerated atherogenesis (i.e. accelerated plaque buildup in the coronary arteries), hypertrophy of the left ventricle, dilated cardiomyopathy, aortic aneurysms, and coronary aneurysms.

Patients who are acutely intoxicated with cocaine and present with chest discomfort should be referred to an emergency room immediately for evaluation. They should undergo a chest-x-ray, an electrocardiogram, blood work to evaluate for evidence of a heart attack and non-myocardial muscle breakdown (e.g. rhabdomyolysis), and to assess kidney function, white and red blood cell counts, and liver function.

Cocaine intoxication is diagnosed if and when patients report recent cocaine use and through serum and urine toxicology screens (which should be performed immediately as well). If a clinician suspects that a patient is acutely intoxicated with cocaine, treatment should not be withheld while waiting for the results of the toxicology screen. Patients with acute cocaine intoxication and symptoms concerning for cerebrovascular or other cardiovascular sequelae of cocaine intoxication may also need additional imaging to assess for evidence of damage to the heart, aorta, or other blood vessels.

In terms of treatment, these patients should receive benzodiazepines to help mitigate the adrenergic surge. If chest pain due to myocardial ischemia is suspected, sublingual nitroglycerin should be administered. Ongoing ischemic symptoms, as well as hypertension and tachycardia (drivers of myocardial oxygen demand) should be treated with calcium channel blockers (i.e. diltiazem or verapamil). Beta blockers should ideally be avoided until there is no cocaine remaining in the patient’s system. If beta blockers must be used, we recommend using either labetalol or carvedilol, which are non-selective inhibitors of both alpha and beta receptors (note: other beta blockers that are selective for beta receptors are contraindicated due to a theoretical risk that selective beta blockade could lead to unopposed alpha-mediated arterial vasoconstriction, which could precipitate marked hypertension and even peripheral and splanchnic ischemia).

Alternative, and highly effective, agents for treatment of hypertension include IV nitroglycerin (which should also be used if the patient has chest pain) and IV nitroprusside. Phentolamine, an alpha blocker, can be used for refractory hypertension. Patients presenting with chest pain should also receive a full dose chewable aspirin (325 mg) and 80 mg of atorvastatin (if available). Patients with ECG changes consistent with myocardial ischemia or infarction and/or elevated blood levels of cardiac biomarkers should be managed identically to patients with non-cocaine induced myocardial ischemia and infarction.

Cocaine and methamphetamine addicts often have heart disease. Why? How is a diagnosis made?Cardiac sequelae are the second most common cause of death (behind overdose) in patients who use methamphetamines (“meth”). Like cocaine use, use of methamphetamines can produce both acute and chronic cardiovascular disease. Acute intoxication with methamphetamines produces a hyperadrenergic state, not unlike having a pheochromocytoma. The hypertension and tachycardia that result can lead to myocardial ischemia and infarction, aortic dissection, malignant arrhythmias, Takotsubo’s (stressinduced) cardiomyopathy, and cardiac arrest.

Chronic methamphetamine use can lead to hypertrophic cardiomyopathy (due to persistent severe hypertension) or dilated cardiomyopathy (due to the drug’s toxic effects on myocardium), and the clinical syndrome of heart failure. In addition, chronic meth use can also cause pulmonary arterial hypertension (PAH). Meth-associated PAH is a devastating disease, with five year mortality rates above 50%.

Diagnosing and managing acute methamphetamine intoxication:

Patients who present with suspected acute methamphetamine intoxication should undergo a full physical exam, electrocardiogram, and basic lab work (including basic metabolic panel, blood counts, clotting times (prothrombin time and international normalized ratio), liver function tests, creatine phosphokinase (CPK), urinalysis, and urine and serum toxicology screens). Amphetamine intoxication or toxicity is ultimately diagnosed by confirming the presence of amphetamines in urine or serum. However, if patients present with signs and symptoms which raise concern for amphetamine intoxication—including hyperthermia, agitation, hypertension, and tachycardia—treatment should not be delayed while waiting for these test results to return.

If there is concern for myocardial ischemia or infarction (for example, if the patient complains of chest discomfort or shortness of breath or the ECG shows ischemic changes), then cardiac biomarkers should be checked as well (i.e. troponin I or T). Acute methamphetamine intoxication with secondary sequelae (i.e. agitation, hypertension, tachycardia) should be managed initially with sedatives (benzodiazepines and 2nd generation atypical antipsychotics).

Hyperthermia should be managed aggressively by controlling core body temperature with sedatives and, if necessary, with paralysis and intubation (but antipyretics should not be used).

Rhabdomyolysis is common, and a CPK level should always be checked in patients who are acutely intoxicated with meth. If the hypertension is refractory to treatment with an adequate trial of sedation, then nitrates and/or phentolamine should be used. Calcium channel blockers can also be used, and are effective agents for managing tachycardia that persists despite sedation. Beta-blockers should be avoided in the acute setting to avoid precipitating unopposed alpha-mediated vasoconstriction (via identical mechanisms to those described above).

If beta blockers are necessary for chronic management of a different disease process (e.g. cardiomyopathy or coronary artery disease), then labetalol or carvedilol are the preferred agents due to their partial alphaantagonism. Myocardial infarction in the setting of methamphetamine intoxication should be managed per evidence-based guidelines for the management of heart attacks, and as described above (for cocaine). The one exception is that, if heart rate control is needed, calcium channel blockers, not beta blockers, should be used. Interestingly, monoclonal antibodies against methamphetamine have been developed and are currently in clinical trials.

Chest pain in the setting of acute methamphetamine intoxication should raise concern not only for myocardial infarction, but also for acute aortic dissection. Methamphetamine abuse is the second most common cause of acute fatal aortic dissection in the US, after hypertension. Unlike chest discomfort due to myocardial ischemia, which often starts as mild or moderate discomfort and worsens progressively over minutes-hours, chest discomfort due to aortic dissection is typically extreme from the outset.

What does the patient PE and EKG look like if a patient has overdosed on opioids? What about when injected with Narcan and reversed? Does Methadone, when given as a MAT, have QT and other effects on the heart? What about Suboxone and the heart?Opiate overdose can precipitate respiratory depression and coma. The pupils will be mioitic, or “pinpoint.” Patients commonly experience mild hypotension as well. The electrocardiogram classically shows sinus bradycardia with nonspecific changes. Approximately 20% of patients will have prolongation of the QT interval. Administration of an adequate dose of Narcan rapidly reverses the respiratory depression, miosis, and coma, and can also lead to improvements in blood pressure and an increase in heart rate.

However, Narcan is short acting and the reversal is temporary. Thus, patients must be monitored following Narcan administration to determine if they need subsequent doses, or even initiation of an IV naloxone drip. Methadone may also cause QT prolongation but is an uncommon cause of Torsades Des Pointes, the potentially fatal arrhythmia that can result from QT prolongation. Suboxone can also cause hypotension, including orthostatic hypotension, and should be used with caution in patients with established cardiovascular disease (e.g. coronary artery disease). However, I am unaware of any unique cardiovascular side effects associated with suboxone use.

Does smoking have effects on the heart?Smoking is an extremely strong and independent risk factor for heart disease, stroke, and peripheral artery disease. Smoking increases the risk of these conditions in a dose dependent fashion, and no amount of smoking is safe. People who smoke less than five cigarettes per day are at increased risk for myocardial infarction relative to non-smokers. The incidence of myocardial infarction among men and women who have smoked at least twenty cigarettes per day for any period of time is three fold and six fold higher, respectively, than the incidence of myocardial infarction in never smokers.

More generally, smoking increases the risk of coronary artery disease, heart attack, arterial aneurysms, aortic dissection, blood clots, carotid artery stenosis, upper and lower extremity ischemic claudication, and death. Smoking’s deleterious cardiac, cerebrovascular, and peripheral vascular effects are the result of a variety of mechanisms that contribute to atherogenesis. Smoking is associated with insulin resistance and oxidization of low-density lipoprotein (LDL-c, or bad cholesterol). Oxidization of LDL-c makes it more proatherogenic. Smoking also activates the sympathetic nervous system which increases heart rate and blood pressure and leads to peripheral vasoconstriction.

What about cannabis addicts or chronic smokers and the cardiologist?While we know relatively less about the effects of marijuana on the cardiovascular system, there is significant and growing interest in understanding how marijuana use impacts heart and blood vessel function. We do know that smoking marijuana leads to an acute, four- to five-fold increase in the risk of myocardial infarction in young men. This risk persists for approximately 60 minutes following inhalation. Daily cannabis use is associated with a 1.5%-3% annual increase in the risk of myocardial infarction. There is some evidence that the mechanism underlying this increased risk is a higher likelihood of experiencing coronary artery vasospasm (as opposed to accelerated atherogenesis).

The physiologic effects of marijuana may surprise some people. Marijuana intoxication typically leads to a slowing of the reflexes, and the appearance of a relaxed state. However, marijuana use actually stimulates the sympathetic nervous system, which leads to tachycardia, the release of systemic catecholamines, and increased myocardial oxygen demand. At the same time, marijuana use increases supine systolic and diastolic blood pressure, and increases the likelihood of experiencing orthostatic hypotension.

There is also some evidence that marijuana use activates platelets by modulating the endocannabinoid system. Longitudinal prospective studies of cannabis users have failed to reveal evidence that chronic cannabis use leads to significant alterations body mass index, blood pressure, total cholesterol, high density lipoprotein, triglycerides, or blood glucose levels. There is no consistent evidence that marijuana use increases cardiovascular mortality. We know relatively little about whether the mode of use (i.e. smoking vs. ingestion) modifies the effects of marijuana on the cardiovascular system.

Ketamine is being used off label for depression. What are the cardiovascular risks and concern when this is done?This is an extremely interesting question. Ketamine is a sympathomimetic. Studies of the cardiovascular effects of Ketamine have found that the drug increases cardiac output by up to 50% in healthy subjects. However, among sicker patients, the drug’s effects appear to be more variable, with some patients experiencing augmented ventricular performance, and others demonstrating some impairment in left ventricular function due to Ketamine use (among coronary artery bypass graft patients, for example, induction of anesthesia with Ketamine has been shown to significantly reduce left ventricular stroke volume).

Ketamine does consistently produce tachycardia and this simple fact should lead us to be cautious about using it to treat depression in patients with obstructive coronary artery disease or congestive heart failure. The cardiovascular effects of Ketamine remain incompletely characterized, and the prospect of widespread use to treat chronic illnesses like depression heightens the need to more clearly elucidate how Ketamine effects the cardiovascular system.

Withdrawal from opioids is associated with hypertension and tachycardia. Is this a concern?Yes—the hypertension and tachycardia which occur during opioid withdrawal can undoubtedly stress the cardiovascular system. Patients with a history of coronary artery disease (particularly those with a history of angina), patients with congestive heart failure, and those with aortic aneurysms should be monitored closely during the withdrawal period for new or worsening cardiovascular symptoms. In addition, patients’ home cardiovascular medication regimens, including beta blockers, antihypertensives, and anti-anginals (i.e. nitrates) should ideally be continued during the withdrawal period if possible in order to blunt the physiologic effects of opioid withdrawal.

Are any drug withdrawal syndromes a concern to a cardiologist?In general, most withdrawal syndromes result in some degree of heightened sympathetic tone, which can produce hypertension and tachycardia. In patients with serious chronic cardiovascular illness, including coronary artery disease, congestive heart failure, valvular disease (i.e. aortic stenosis, mitral stenosis, or mitral regurgitation), or arrhythmias, including atrial fibrillation or paroxysmal supraventricular tachycardia, this sympathetic surge can precipitate symptoms or even acute decompensations. So, and this is a key point, it is the patient substrate which matters more than the specific withdrawal syndrome. Put another way, if the patient has significant cardiovascular comorbidities, any withdrawal syndrome may be dangerous.

In general, I worry most about alcohol withdrawal for a few reasons. First, alcoholics regularly live with multiple comorbidities, including cardiovascular comorbidities like atrial fibrillation and heart failure (which may be due to an alcoholic cardiomyopathy). I have seen alcohol withdrawal precipitate new or recurrent atrial fibrillation, and lead to acute heart failure decompensations in patients with underlying alcoholic cardiomyopathies.

Second, alcohol withdrawal is by far the most mortal withdrawal syndrome; seizures due to withdrawal, or delirium tremens, carry a significant risk of mortality in patients without underlying cardiovascular illness, and may be even more dangerous in patients who are suffering from concomitant cardiovascular disease. Third, many alcoholics are poorly nourished, and have significant electrolyte disturbances, including hypokalemia (which is a risk factor for ventricular arrhythmias).

The wasting of magnesium that occurs in alcoholics is particularly concerning, because potassium repletion is ineffective in the absence of adequate serum magnesium levels. Thus, when checking basic electrolytes in an alcoholic (e.g. sodium, potassium, bicarbonate, chloride, etc.), be sure to also check magnesium levels. And, if an alcoholic is hypokalemic and you don’t have a serum magnesium level, replete the magnesium before giving potassium (or alongside the potassium). A little extra magnesium won’t have any adverse consequences, but failing to replete magnesium could result in failure to correct the low potassium level, which could have serious consequences.

Which patients should an addiction rehab send to a cardiologist for evaluation?This is a difficult question to answer with high specificity. First, any patient with new or concerning cardiovascular symptoms or confirmed cardiovascular disease, including 1) exertional chest discomfort; 2) documentation of a new or recurrent arrhythmia; 3) new exertional shortness of breath; and/or 4) new signs or symptoms of congestive heart failure, including exertional shortness of breath, new or progressive lower extremity edema, and/or paroxysmal nocturnal dyspnea or orthopnea, should be evaluated by a cardiologist. In addition, anyone with a syncopal event without a prodrome (i.e. sudden, unexplained, and unheralded syncope) or with a history of complex congenital heart disease should be referred to see a cardiologist.

Patients with chronic, stable cardiovascular comorbidities, including coronary artery disease (with or without angina), congestive heart failure, peripheral artery disease (with or without claudication), valvular disease (i.e. aortic stenosis or mitral regurgitation), and/or cerebrovascular disease do not necessarily need to be seen by a cardiologist while they are in Rehab, and provided they remain stable and are able to continue their long term outpatient treatment regimens for these conditions. However, a rehab should generally have a low threshold to engage a cardiologist in the management of any patient with complex, chronic cardiovascular disease.

What are the CVD effects of alcohol use, abuse, and addiction? Alcohol users have a variety of CV effects including noticing that their heart skips a beat or so…is this related to alcohol abusers or alcoholics heart blocks?Modest alcohol consumption—two or fewer drinks per night for a man, and one drink per night for a woman— has been shown to be healthy, and may even reduce all-cause mortality and mortality due to cardiovascular disease. However, when consumed in greater quantities, alcohol is a cardiotoxin. People who abuse or are dependent on alcohol have a heightened risk of arrhythmias—including atrial fibrillation, atrial flutter, and ventricular arrhythmias (due to electrolyte abnormalities or an alcoholic cardiomyopathy)—and alcoholic cardiomyopathy.

Alcoholic cardiomyopathies can be profound; I have taken care of daily drinkers who present with severe, bi-ventricular dysfunction and left ventricular ejection fractions (LVEF) of 10%-15% (normal is 52- 70%). Importantly, alcoholic cardiomyopathy is usually not this fulminant. Many daily drinkers may suffer from very mild, and even subclinical, forms of this cardiomyopathy, and their LVEF may be normal.

However, in these patients the cardiotoxic effects of alcohol may still predispose to premature atrial and ventricular beats—which they may experience, and describe, as “skipped beats.” As noted above, alcoholic cardiomyopathy increases the risk of both atrial and ventricular arrhythmias, and prior work shows that the risk of ventricular tachycardia in alcoholic cardiomyopathy is comparable to that seen in patients with idiopathic dilated cardiomyopathies. The electrolyte abnormalities commonly found in alcoholics—most notably hypomagnesemia and hypokalemia— further compound the risk for these arrhythmias.

Fortunately, alcoholic cardiomyopathy is usually a reversible process; I have multiple patients whose LVEF has improved from this 10%-15% range (while drinking daily) to 50% or more (essentially normal) after one-two years of abstinence from alcohol and adherence with traditional heart failure therapies. Alcoholic cardiomyopathy may at times reach a point of irreversibility, of course, but, broadly speaking, it has a very favorable prognosis if long term abstinence can be achieved.

Alcoholic abuse/dependence is also associated with a modestly increased risk for myocardial infarction, particularly in patients with pre-existing cardiovascular disease.

I’m sure the good people at the Health Service Executive were trying to be all mature and socially relevant about Ireland’s growing cocaine problem when they issued their “harm reduction” guidelines recently on how to make taking the drug safer. But they weren’t. Worse still, they were being flippantly irresponsible.

Cocaine usage in the country is now back to Celtic Tiger-era levels – a time when it was commonplace in Dublin night spots to see one of our wretched “media personalities” furiously rubbing their nose to indicate to everyone that they had just snorted something resembling cocaine – but was more likely a baking soda cocktail that would only give them diarrhoea.

To tackle this new reinfestation of the “VIP” drug, the HSE tells us that in order to reduce the risks posed by taking cocaine, users should avoid mixing it with alcohol. Which would lead you to wonder if anyone at the HSE has being out socially in Dublin – ever?

“Cocaine has enough good PR without the HSE offering tutorials (particularly to first-time users – invariably youngsters) on how and when to take it”

They also advise that we should always know the source of our cocaine when buying it. Do the people at the HSE actually know there’s a difference between buying a cup of hipster coffee and half a gram of cocaine? Why not ask the dealer if it’s Free Trade, organic cocaine while you’re at it?

They add that cocaine users should start with a small test dose and wait two hours before taking any more. Seriously? Having an allergic reaction to what passes as cocaine in Ireland would be the least of your worries here.

They also recommend that the powder should be ground up finely so that you won’t be snorting lumps. The HSE really should have their Netflix subscription cancelled.

If the HSE is genuinely interested in “harm reduction” when it comes to the use of cocaine, it could have simply pointed out that the drug is as unethical and immoral as they come. Between its provenance and its distribution, it is inextricably linked to death squads, the merciless exploitation of children and rapacious organised crime.

HSE’s Dr Eamon Keenan, Minister of State Catherine Byrne and Tony Duffin of Anna Liffey: If the HSE is genuinely interested in “harm reduction” when it comes to cocaine, it could have pointed out the drug is unethical and immoral.

Celtic Tiger years

Cocaine has enough good PR without the HSE offering tutorials (particularly to first-time users – invariably youngsters) on how and when to take it.

An insidious link has been made between the drug and status/success – cocaine became, during the Celtic Tiger years, a signifier that not only had you made it but, rather pathetically, that you were also “edgy and exciting”. As edgy and exciting as taking a drug known – for good reason – as “middle-class Bostik” can ever make you.

There is no gainsaying cocaine’s meretricious attraction. Sigmund Freud spoke of the “exhilaration and lasting euphoria” he got from taking it and how it facilitated “more vitality and capacity for work”.

Naomi Campbell spoke of how “cocaine made me feel invincible, like I could conquer the world”; Stephen King how it “ just owned me body and soul. Once cocaine was there it was like the missing link – click! – like when you turn on lights.”

It is also one of the most effective appetite-suppressants available.

But it also a potentially fatal toxin, that runs riot with your brain chemistry, heart rate and respiratory system. Use of the drug is followed by a highly unpleasant “crash” sensation – as debilitating psychologically as it is physiologically. And financially.

Murderous journey

As Naomi Campbell and Stephen King learned the hard way: cocaine eats you from the inside out. Recovering cocaine addict TV presenter Trinny Woodall put it best when she said of her habit: “I wanted to be cool. Instead I became a fake, lying, thieving cheat.”

Because cocaine usage in developed countries is, according to most reliable data, associated with the professional classes, it is mordantly amusing to find that those who profess to being environmentally and politically aware are so selfishly oblivious to the murderous journey the gram of cocaine at their summer BBQ has been on.

The only proven way to effectively reduce cocaine use among the demographic that consume it most is to educate them about the social, political and economic iniquities it reinforces and shame them out of their reckless stupidity.

Once, people would attract admiring looks and comments for wearing a fur coat; you run the risk of getting spat at in the face if you wear fur these days. Cocaine needs to be hurried along on that journey.

Having our Health Service Executive tell us how to grind our cocaine is like something out of Ali G. Grow up HSE and tell the truth about this grubby little drug.

Childhood adversity permanently alters the peripheral and central immune systems, increasing the sensitivity of the body’s immune response to cocaine, reports a study by researchers at the IRCCS Santa Lucia Foundation and University of Rome “La Sapienza,” Italy.

The study, published in Biological Psychiatry, showed that exposure to psychosocial stress early in life altered the structure of immune cells and inflammatory signals in mice and led to increased drug-seeking behavior. Exposure to early psychosocial stress in mice, or a difficult childhood in humans, increased the immune response to cocaine in adulthood, revealing a shared mechanism in the role of immune response in the effects of early life stress on cocaine sensitivity in mice and humans.

The findings help explain why as many as 50 percent of people who experience childhood maltreatment develop addiction problems. The results in mice and humans suggest that exposure to adversity during childhood triggers activation of the immune system, leading to permanent changes that sensitize the immune system and increase susceptibility to the effects of cocaine in adulthood.

“This paper suggests the existence of an extraordinary degree of interplay between the neural and immune systems related to the impact of early life stress on later risk for cocaine misuse. It both highlights the complex impact of early life stress and suggests an immune-related mechanism for reducing later addiction risk,” said John Krystal, MD, Editor of Biological Psychiatry.

After inducing psychosocial stress in 2-week-old mice by exposing them to a threatening male, first author Luisa Lo Iacono, PhD, and colleagues examined brain immune cells, called microglia, in adulthood. Early social stress altered the structure of microglia in the ventral tegmental area, a brain region important for the reward system and drug-seeking, and increased the response of microglia to cocaine. In the peripheral immune system, early social stress increased the release of inflammatory molecules from white blood cells, which was further amplified by exposure to cocaine, compared with control mice.

“Remarkably, pharmacologically blocking this immune activation during early life stress prevents the development of the susceptibility to cocaine in adulthood,” said senior author Valeria Carola, PhD. Mice who received an antibiotic to prevent activation of immune cells during social stress did not have cellular changes or drug-seeking behavior.

The study also compared immune system function of 38 cocaine addicts and 20 healthy volunteers. Those who experienced childhood maltreatment had increased expression levels of genes important for immune system function. And the highest levels were found in cocaine addicts who had experienced a difficult childhood.

The findings add to the growing collection of evidence from the research group for the negative effects of early life trauma on brain development. “Our work emphasizes once again the importance of the emotional environment where our children are raised and how much a serene and stimulating environment can provide them with an extra ‘weapon’ against the development of psychopathologies,” said Dr. Carola.

A fall in the price of cocaine has led to the highest number of young people using class A drugs in more than a decade, experts say.

Cocaine prices are at their lowest levels in more than 25 years and young people are finding Class A drugs easily accessible, charities warned. The drug is more widely available thanks to mobile phones and is being distributed to users outside city centres thanks to “county lines” in which gangs use children to export their trade to suburban and rural areas.

Figures released by the Home Office from the Crime Survey of England and Wales for 2017/18 show that 8.4 per cent of 16 to 24 year-olds had used Class A drugs in the last year, compared to seven per cent in 2016/17.

The proportion is the highest since 2005/6 and a significant rise from the recent low of 4.8 per cent, seen in 2012/13. Six per cent had used powder cocaine, up from 4.8 per cent in the previous year and the highest figure since 2008/2009.

Figures from the UN’s 2018 World Drug Report show that in 2016 the street price of a gram of cocaine in the UK was $54 (£41), the cheapest at any point since 1990, when the time series begins. In 2007 the price was $91 (£69), and prices climbed as high as $128 (£97) in 1998.

Yasmin Batliwala, chair of London-based drug and alcohol treatment charity WDP, said young people were paying as little as £30 for a gram.

“Our young people’s services have seen a significant rise in the use of Class A drugs. The primary drug of choice has always been alcohol, as well as cannabis, but certainly in the last two or more years the use of Class A drugs has increased substantially. “Class A drugs such as cocaine are extremely easily available. It’s actually very difficult to avoid drugs these days.In terms of price the cost has come down, so they’re not that expensive,” she said.

Harry Shapiro, of DrugWise, said the lower price of the drug meant users no longer had to be “city boys with lots of money”. Mobile phones also made it easier for people to “hook into a regular supply,” he said. “You’ve got a broader network of distribution making it available in places where it wasn’t before, and they don’t have to hang around on street corners waiting for a bloke any more.

“Some people have got their dealer on speed dial and it’s a bit like home delivery of pizza. All of that allows for a more discreet, wider network of distribution.”

Earlier this month addiction charity Addaction said its drug workers were dealing with children as young as 13 who were addicted to cocaine. The organisation said the issue was a particular problem in Scotland, where its South Lanarkshire service has lowered the age threshold of its services from 14 to 13.

One of the charity’s workers Jacqueline Baker-Whyte said: “In the past, cocaine was a drug for people with money. That’s no longer the case. It’s cheap, plentiful and easy to get. The ‘quality’ is usually poor and the side effects can be horrendous.”

A spokeswoman for drugs charity Release said the figures showed that “criminalisation does not deter drug use”.“The reported increase in recent powder cocaine use could be attributed to the drug’s reduced street-level price, and its higher purity,” she added.

A Staffordshire bull terrier that mauled its owner to death while taking part in a BBC documentary had eaten a stash of crack cocaine, an inquest was told.

The dog, named Major, repeatedly bit the throat and face of its owner Mario Perivoitos, an IT expert, in front of a two-man crew from the BBC show Drugs Map Britain shortly after filming.

The crew managed to lock the dog in another room and call an ambulance but Mr Perivoitos died at the scene. The animal was found to have taken enough drugs to put a human eight times over the drug-drive limit.

North London coroner’s court was told that Mr Perivoitos, 41, was a heroin user and had suffered an epileptic fit before the dog set upon him at his flat in Wood Green, north London.

Jessica Winteringham, the assistant producer, said that after the crew had finished filming, Mr Perivoitos had appeared angry, before becoming unresponsive and lying on the bed next to the dog. “Then the dog got up and got his right cheek and then his left and then clamped on to his neck,” she said. “We were shouting ‘no Major’ to try and stop him. Mario did not make any attempt to move or do anything.”

Joshua Haddow, the show’s producer, said he struggled to pull Major off its owner: “I just started hitting the dog, I just did not know what else to do and as I did that it started to loosen its grip.

“I picked it up by the scruff of its neck and I threw it into a room . . . the idea being that I shut the door and I went back to Mario to try and see if we could do anything. The dog was very peaceful, it was friendly with us, it would lick our hands and say hello, there was no way we could have pre-empted it.

“When Mario disturbed the dog on the bed he was behaving quite strangely, the dog was relaxing, he essentially clambered and disturbed the dog, he started to nip his face at first a little bit and then it quickly escalated.”

Nicholas Carmichael, an expert in veterinary toxicology, said cocaine and morphine were found. “It is very likely that this dog had consumed drugs, probably eaten them. It is almost impossible to say whether that will make the dog attack. The dog was eight times the drug-drive limit.”

Andrew Walker, senior coroner, recorded a conclusion of death as a consequence of injuries received from a dog.

* Patients who received transcranial magnetic stimulation (TMS) were more likely to abstain from cocaine than patients who received medications for symptoms associated with abstinence.

* Researchers concluded that TMS appears to be safe and its efficacy as a treatment for cocaine addiction deserves to be evaluated in a larger clinical trial.

Transcranial magnetic stimulation (TMS) projects electromagnetic fields into the brain and can be used to either increase or decrease neuronal responsiveness in targeted brain areas. Researchers have hypothesized that administering TMS to strengthen activity in the prefrontal cortex (PFC) and downstream brain regions can alleviate cocaine addiction (see Narrative of Discovery: Can Magnets Treat Cocaine Addiction?). Previous findings that support the hypothesis include:

* Studies in animals and people have demonstrated that exposure to cocaine weakens neuronal activity in the PFC, and have linked that decreased activity to some of the primary manifestations of addiction, such as craving and compulsive drug-seeking.

Figure. Patients Receiving TMS for Cocaine Addiction Achieve Higher Rates of Abstinence During a 21-day assessment period, higher proportions of TMS-receiving patients than of control patients always gave urine samples that tested negative for cocaine. At completion of the assessment period, 69 percent of those treated with TMS had been continuously abstinent from cocaine versus 19 percent of control patients.

A new pilot trial sets the stage for testing the hypothesis definitively in a large-scale placebo-controlled clinical trial. In the trial, Dr. Antonello Bonci of NIDA’s Intramural Research Program, Dr. Alberto Terraneo, Dr. Luigi Gallimberti and colleagues in Italy and the United States, administered a 29-day course of TMS to 16 patients in an outpatient clinic in Padua, Italy. Of the 16, 11 (69 percent) produced 6 cocaine-negative urine samples, and no positive samples, during a 21-day assessment period that started on treatment day 9 (to allow cocaine that the patients had taken before the study to clear their systems) (see Figure). Among a comparison group of 16 patients who received only medications to control symptoms of depression, anxiety, and insomnia, only 3 (19 percent) made it through the assessment period without using cocaine. The TMS-treated patients also reported less craving for cocaine.

In a second phase of the trial, the researchers administered TMS to 10 patients from the original comparison group, 8 of whom had used cocaine during the first phase. Of the

10, 7 (70 percent) then were followed for 63 days post-TMS and achieved abstinence—an outcome nearly identical to that of the patients who received TMS in the first phase.

The researchers have maintained contact with most of the patients in the study. Dr. Bonci says, “While this observation is not part of a rigorous clinical trial follow-up, and should be taken cautiously, the majority of patients who achieved abstinence during the stimulation pilot protocol report that they have maintained that abstinence for more than 2 years. During that time, some patients have requested additional TMS therapy once a week, twice a month, or monthly, and patients can always request additional therapy if they experience cravings. Others report that they have maintained abstinence without additional TMS after the initial set of treatments.”

Aiming and Tuning the Machine

Dr. Terraneo and colleagues’ protocol focuses the TMS electromagnetic field on the left dorsolateral region of the patients’ PFC. Dr. Bonci explains, “This region is accessible and is involved in a number of addiction processes.” In particular, it has been strongly associated with drug craving. In contrast, he adds, “Stimulating the right side can cause anxiety or discomfort in some patients.” (See “A Case for Studying Brain Asymmetry in Drug Use”).

The researchers set the TMS machine to emit magnetic pulses with a frequency of 15 Hz and an amplitude based on each patient’s baseline neuronal responsiveness. The treatment schedule was designed to induce enduring, rather than brief, increases in neuronal responsiveness. Patients underwent TMS on 5 consecutive days during the first study week, then once during each of the remaining 3 study weeks. Each session lasted 13 minutes, during which the patient’s brain was exposed to 2,400 pulses.

Dr. Bonci emphasizes the safety of TMS: “Properly administered, TMS is very safe. The magnetic pulses are much weaker than those generated in an MRI.” Some patients have experienced headaches or pain at the site of stimulation in the first couple of sessions, but, these adverse effects are generally mild and temporary. Dr. Bonci says, “Few medications have such mild side effects.”

The researchers are planning a larger trial with a more rigorous design, which will address some considerations that limit the interpretation of this pilot trial. Because patients’ responses in the pilot trial may have been influenced by knowing whether they were getting TMS or medication, all patients in the new trial will receive either active TMS or sham TMS without knowing which. The new trial will also examine the possibility that TMS helped participants in the pilot trial abstain from cocaine by reducing depression that is experienced by many cocaine users. Dr. Bonci says, “This region [the dorsolateral PFC] has been a TMS target for the treatment of depression for many years.”

“Most likely, TMS should be coupled with behavioral interventions and medication. I would expect a beneficial synergistic effect. Medication may be particularly necessary for difficult cases when TMS alone is not sufficient,” Dr. Bonci adds. Dr. Harold Gordon, of NIDA’s Epidemiology Research Branch, emphasizes the potential clinical advantages of TMS. “A non-pharmaceutical treatment for addiction would be not only cost-effective but patient-friendly in terms of both compliance and convenience.”

New research from the Icahn School of Medicine at Mount Sinai using electroencephalography, or EEG, indicates that adults addicted to cocaine may be increasingly vulnerable to relapse from day two to one month of abstinence and most vulnerable between one and six months. The findings, published online today in JAMA Psychiatry, suggest that the most intense periods of craving for illicit substances often coincide with patients’ release from addiction treatment programs and facilities.

It is not known why individuals with substance use disorders relapse even after remaining abstinent from illicit substances for long periods of time. However, it is clear that cue-induced craving—craving elicited by the exposure to cues previously associated with drug use—plays a major role in relapse. Until now, studies have used self-reported measures to assess cue-induced craving. This is the first study that uses EEG to quantify cue-induced craving in humans with cocaine use disorder, showing a similar trajectory of craving demonstrated in previous studies using animal models. In this study and in contrast to the EEG measures, self-reported craving showed a gradual decline with increasing abstinence duration, underscoring a potential disconnect between the physiological response to drug-related cues in addicted individuals and their perception of this response.

“Our results are important because they identify an objectively ascertained period of high vulnerability to relapse,” says Muhammad Parvaz, PhD, Assistant Professor of Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, and the study’s lead author. “Unfortunately, this period of vulnerability coincides with the window of discharge from most treatment programs, perhaps increasing a person’s propensity to relapse.”

Over five and a half years, the research team collected data from EEG recordings in 76 adults addicted to cocaine with varying durations of abstinence (two days, one week, one month, six months, and one year). EEG was recorded while participants looked at different types of pictures, including pictures that depicted cocaine and individuals preparing, using, and simulating use of cocaine. After EEG, participants also self-rated their level of craving for each cocaine-related picture.

“Results of this study are alarming in that they suggest that many people struggling with drug addiction are being released from treatment programs at the time they need the most support,” said Rita Goldstein, PhD, Professor of Psychiatry and Neuroscience at the Icahn School of Medicine and Principal Investigator of the study. “Our results could help guide the implementation of alternative, individually tailored and optimally timed intervention, prevention, and treatment strategies.”

A few years ago Dr. Diana Martinez and Dr. Marco Diana decided to investigate a new technology that uses magnetic pulses to stimulate brain cells. Both had been trying to develop medications to treat cocaine addiction, and both had come to feel that the pace of progress—their own and others’—was unequal to the urgency of the need. In the new technology, transcranial brain stimulation (TMS), they saw a potential treatment that might be developed relatively rapidly for clinical use.

Dr. Martinez, a neuroimaging specialist at Columbia University Health Center in New York City, planned a preclinical study. She was using a relatively new type of TMS coil (magnetic pulse generator), and her first objective was to identify machine settings with potential clinical efficacy.

Participants in her study were cocaine users who did not want to stop. They came into the hospital research unit, and attended a self-administration session in which they repeatedly chose between smoking a dose of the drug and receiving a sum of money. They then underwent TMS for 3 weeks, after which they repeated the self-administration session. If they chose cocaine less often after treatment than they had before, the setting that was used would be a good candidate for further testing.

Dr. Diana, a research pharmacologist at the University of Sassari, Italy, designed a pilot clinical trial. Sixty people who were trying to quit cocaine would receive TMS, real or sham, every other day for a month. Dr. Diana would assess their cocaine use though interviews and hair analysis before they started TMS, at the end of the treatment month, and every 3 months thereafter for a year. He hoped that the patients who received real TMS would reduce their cocaine use.

Both researchers’ projects hit snags early on. In this installment, we follow Dr. Martinez as she resolves an initial impasse and advances her project to a new stage. Meanwhile, circumstances close in on Dr. Diana. He is forced to cut short his trial, but comes away with encouraging data and increased enthusiasm for TMS.

Frequency and Intensity

The first TMS settings Dr. Martinez tested appeared to reduce cocaine intake among participants who completed the course of treatment. However, only one third completed the course. The rest complained of pain and anxiety during their first treatment session, and refused to continue.

Dr. Martinez adjusted one of her settings to try to prevent patient dropout. Reducing the magnetic pulse frequency from 10 Hz to 1 Hz abolished the aversive responses, but also the reductions in cocaine use.

Dr. Martinez considered testing an intermediate frequency. In the end, she decided to look for a way to make 10 Hz more tolerable. She says, “If you look at the literature on TMS in psychiatric disorders, there’s a strong rationale for using 10 Hz, or even 15 or 20 Hz.”

She asked herself why so many participants hadn’t tolerated TMS at 10 Hz, when many other researchers had used it without problems. Of several possible explanations, one stood out: Cocaine users tend to have exceptionally high motor thresholds.

Dr. Martinez explains, “A person’s motor threshold is the lowest TMS intensity that will stimulate his or her motor neurons to fire and contract a muscle. The TMS technician ascertains the motor threshold to determine how much stimulus to apply in treatment. If the stimulus is strong enough to activate motor neurons, it’s presumably enough to activate neurons in other cortical areas as well.”

To ascertain the motor threshold, the technician directs the TMS pulse at an area of motor cortex that controls a muscle, for example a hand or calf muscle. The technician delivers a pulse at a low intensity setting, then dials the intensity up in small steps until the target muscle twitches. The twitch gives visible proof that motor neurons have fired.

Dr. Martinez says, “The motor thresholds of the cocaine users in our study were in the range of 80 percent to 84 percent of the power output of our TMS coil. That’s higher than the thresholds that have been recorded in other studies with coils of this type. It’s also been reported in the literature that cocaine users have high motor thresholds.”

Because of their high motor thresholds, Dr. Martinez’ study participants received exceptional amounts of stimulation during the ascertainment procedure. She says, “We had to keep turning up the intensity of the stimulus, and it would often take us a good 40 minutes to work up to the threshold.” Maybe, she thought, so much stimulation during the ascertainment, plus the additional stimulation applied during treatment, hyper-excited neurons in a way that caused pain and alarm.

Dr. Martinez tested her conjecture on herself. She recounts, “When we first started working with TMS, I was curious about the experience, so I went under the coil to ascertain my motor threshold. I found out that, like cocaine users, I tend to have a higher threshold than the average person. During the ascertainment procedure I developed a headache and some other mild symptoms, but nothing too unpleasant. Now I decided to see how I would feel if I underwent what our study participants were getting—motor threshold ascertainment followed by a 10-Hz treatment. I was miserable.”

Tweak and Succeed

Dr. Martinez considered how she might adjust her study protocol to make TMS at 10 Hz comfortable for cocaine users despite their high motor thresholds. She could obtain no guidance from colleagues or the scientific literature, because no one had ever before used the specific TMS coil she was using, called the H coil, with cocaine users.

Dr. Martinez turned for advice to Dr. Abraham Zangen, of Ben-Gurion University of the Negev, in Israel, a researcher and developer of the H coil. Brainstorming together, the two came up with two adjustments:

* Dr. Martinez had been administering TMS treatment directly after motor threshold ascertainment. Going forward, she would separate the two: ascertain the motor threshold in the morning and deliver treatment in the afternoon. Doing so would spread the stimulation over a longer time.

* She would lower the intensity of the TMS treatment. Dr. Zangen had been using the H coil to treat patients with obsessive compulsive disease, and had found that intensities lower than the motor threshold could be effective.

Dr. Martinez says that when she returned to the TMS laboratory, “We weren’t sure that these adjustments would work. We were nervous. And the participants picked up on our unease. They were looking at us like, ‘Why are you nervous?'” The adjustments worked (see Figure). Participants no longer reported pain, and most now stayed on to complete the treatment. A further protocol adjustment—spreading motor threshold ascertainment over 4 days—further increased the completion rate.

Dr. Martinez says, “These adjustments to our protocol give people time to acclimate to the stimulation. We’ve seen that TMS definitely gets less painful over time.”

With the amended protocol, Dr. Martinez quickly reached her goal of treating 6 participants with TMS at 10 Hz. These patients reduced their choices for cocaine, from about 5.5 before the treatment to 2.2 after it. No changes in the choice for cocaine were seen in the groups that received sham or low-frequency TMS.

Dr. Martinez says, “I must thank Dr. Zangen, who spent a lot of time discussing ways to fix my protocol. I’m also grateful to Brainsway Corporation, makers of the H coil, who have a real interest in treating addiction, and provided me with the equipment to do this work.”

Judging that she had enough evidence that her TMS protocol was efficacious to warrant a pilot clinical trial, Dr. Martinez began to prepare a grant proposal. In the next installment of this Narrative of Discovery, we’ll follow Dr. Martinez into this next stage of her project.

Figure. TMS Frequency and Intensity Settings Determine Efficacy and Tolerability In Dr. Martinez’ study, participants who completed a course of TMS with a frequency of 10 hertz (Hz, pulses per second) (A) reduced their cocaine use, but many found the treatment intolerable. Participants tolerated TMS with a frequency of 1 Hz well (B), but did not reduce their cocaine use. Dr. Martinez adjusted the schedule of her TMS protocol and tried 10 Hz again, this time with success. For her final settings, she also lowered the TMS pulse intensity (amplitude) from 120 percent of motor threshold to 110 percent of motor threshold (C).

Bad News

Dr. Diana’s recruitment effort ran into a deep fund of suspicion. When Dr. Diana showed potential trial participants the TMS machine and explained its purpose, many accused him of intending to subject them to electroshock. Some declined to participate. In 2 years, he enrolled only 20 patients.

In mid-2015, Dr. Diana applied to the Italian Department of Anti-Drug Policies for an extension of his funding for the project. Weeks, then months, passed with no response. Dr. Diana’s remaining funds from the past year dwindled. In July, he stopped recruiting patients because he was out of money to pay the laboratory to test hair samples for cocaine metabolites. He continued to provide his existing patients with psychological support and ask them about their cocaine use. Without biological confirmation, however, the scientific community would accord less weight to his patients’ self-reports.

“Finally, in November, the Agency was forced to respond because I was making thousands of phone calls,” Dr. Diana says. “I reminded them that we knew from the start this was going to be a 3-year project. It would be a shame not to finish, because we had encouraging preliminary findings. They told me, ‘Look, we wish you all the luck you certainly deserve, but we don’t have money to give you.”

Striking the Tent

Unable to continue his study, Dr. Diana set out to reap what he could from his years of work. He had administered real or sham TMS to 19 patients, far short of the 60 he needed to establish that his TMS approach was effective. “I can’t do any statistics on such a small number and hope to persuade my colleagues that our findings are predictive,” he says.

Nevertheless, Dr. Diana says, “We didn’t have any choice. We had to either analyze our data and see what was there or just throw everything out.” Although he could prove nothing with results from so few patients, at least he would find out if their outcomes were consistent with TMS being effective. If they were, his work might inspire others to try TMS.

The outcomes were indeed consistent. Patients in both the TMS- and sham-treated groups were using less cocaine 1 and 3 months after starting the treatment. The difference in the amount of reductions was not statistically significant, but a significant difference emerged at the 6-month follow-up. At that time, the patients in the TMS-treated groups were using about 70 percent less cocaine than they had before starting the trial, and the sham-treated group about 45 percent less.

In addition, Dr. Diana says, “The study participants commonly reported that their mood was much better. They were more comfortable with life. They didn’t feel overwhelmed with guilt. Their anxiety levels went down significantly after the treatment. Some also described regularization of sleep, with better circadian rhythms.”

For Dr. Diana, the persisting effect of TMS past 6 months hints that his most ambitious hope for TMS may pan out: The treatment may not just temporarily remit cocaine addiction, but actually restore the patient’s brain to a pre-addicted state (see “Can Neurons Be Reeducated?”).

Enthused and wishing to share his findings, Dr. Diana wrote a report to submit for publication. He knew the chances were slim that a journal would accept it. As of this writing, one journal has turned down the manuscript, and Dr. Diana awaits a decision from a second journal. (Update: In July 2016, Dr. Diana’s manuscript was accepted for publication in the journal Frontiers in Psychiatry−Addictive Disorders.)

Lessons and Plans

Dr. Diana sees his loss of funding in perspective. He notes that Italy is experiencing tight economic times and the government has reduced its investment in research: “We have a new prime minister who looks very efficient, very pragmatic. Everybody seems to be reporting that the country’s situation is improving economically. But when you apply for funding for research, many times the answer you get is, ‘We are now fixing things more important than research.’ Unfortunately, they don’t understand that it’s through research and innovation that you generate more jobs and well-being for people.”

Dr. Diana’s broad perspective has not precluded disappointment. He says, “I worked on this study for five years. Before I even started to recruit patients, I worked 2 years to get it approved by the ethics committee and the hospital director, plus paperwork for this and that, endless paperwork. So it’s very frustrating. But what can I say?” Despite his disappointment, Dr. Diana remains excited about TMS. He has already teamed up with a collaborator, Dr. Giorgio Corona, in Cagliari, Sardinia. “We are set to continue this work and to replicate my observations with a larger sample,” Dr. Diana says.

For Dr. Diana, starting over, although far from what he would have wished, presents opportunities to implement new knowledge and lessons learned. In his new trial, for example, he will measure patients’ central dopamine levels, using a technique that came to his attention too late to be used in his previous trial (see “Windows Into the Brain”).

The new trial’s recruitment protocol will incorporate another lesson, this one learned at great cost: To put to rest misperceptions and mistrust, potential recruits will receive a thorough orientation designed to put them at ease about TMS. Dr. Diana says, “Our strategy will be to persuade patients that TMS really is safe and without side effects. We’ll show them the machine. We’ll show them videos of other people who have taken the treatment. And we’ll tell them that if they perceive anything is wrong, they can leave the study whenever they decide.”

Dr. Diana is eager to get his new trial underway. He says, “The idea that TMS can be useful has been reinforced in me. Comparing the effects we observed with TMS to what others are reporting with medications, I think TMS is the way to go. The new machine is being delivered as we speak.”

Can Neurons Be Reeducated?

Dr. Diana explains, “We know from studies by Nora Volkow, Diana Martinez, and others that cocaine use over time weakens dopamine neurons. These neurons fire less often and less vigorously in the addicted brain, and this accounts for a person’s cocaine craving and compulsive responses to cocaine cues. We administer TMS to increase those neurons’ firing rate and strength back to their pre-cocaine levels. That might be therapeutic, but it won’t be so great if the neurons just revert to their weakened state after the treatment, and the patient has to keep coming back indefinitely. We want an effect that lasts for a long time.

“Therefore our aim with TMS is to induce an effect called long-term potentiation, LTP, of the dopamine neurons. LTP is something that occurs naturally when a neuron repeatedly receives intense high-frequency stimulation from other neurons. The neuron develops structural changes that make it more active and sensitive to future stimulation, and that endure for extended periods.

“In my personal opinion, the results of my trial, although they are preliminary, indicate that TMS produced LTP of our patients’ dopamine neurons. Our TMS-treated patients continued to use much less cocaine for 5 months after our 1-month treatment. The contrast in outcomes between our TMS-and sham-treated groups also supports this idea. We think that the sham TMS had a strong placebo effect that lasted 2 months after the treatment, possibly because the experience of sitting under the apparatus makes a powerful impression. After 5 months, however, the placebo effect began to wear off, while LTP kept the neurons in the TMS-treated group strong.’

Dr. Diana adds, “With TMS we were trying to tell the dopamine neurons, ‘Okay. You fire faster, and remember that you are able to fire faster.’ I think the neurons got the message.”

Windows Into the Brain

The underlying idea of using TMS to treat cocaine addiction is that stimulation with magnetic pulses can re-invigorate hypofunctional dopamine signaling in the prefrontal cortex. To make the best case for TMS’ efficacy, Dr. Martinez and Dr. Diana would like to show not only that TMS reduces cocaine use, but also that the reductions are paralleled by increases in dopamine. Retinography is a tool—albeit a tricky one—for accomplishing this. With retinography, researchers measure dopamine levels in the retina, and interpret them as indicators of levels in other parts of the central nervous system.

Over the past decade drug use has fallen significantly according to the annual Crime Survey of England and Wales.

Stronger ecstasy is tempting some users back to the market

But figures published by the Home Office suggested the group bucking that trend are the professional middle classes with household incomes in excess of £50,000 a year.

It comes as statistics from the Health and Social Care Information Centre showed that the number of deaths from illicit drug use was at its highest level since 1993.

The number of hospital admissions for drug related poisoning was also up 57 per cent on the previous decade.

Three per cent of people aged between 16 and 59 with a household income higher than £50,000 admitted taking cocaine over the past 12 months, up from 2.2 per cent the previous year; while 2.2 per cent admitted taking MDMA or ecstasy, up from 1.5 per cent in 2014.

However the figures for people from lower income households suggested that their use of the deadly Class A drugs were down year on year.

This comes despite a high profile campaign by the police to warn the middle classes that they were being targeted in the war on drugs. Bernard Hogan-Howe, the Commissioner of the Metropolitan Police, recently said affluent people who indulged in cocaine use at home, were fuelling the £1 billion market deadly drugs market.

He even suggested that employers should consider introducing regular drug testing as a condition of employment.

But experts believe the warnings have done little to deter the middle classes, who have been tempted into taking drugs because of an improvement in quality.

Niamh Eastwood of the charity Release said: “We know from experience that legislation does not have a significant impact on drug use, but this is particularly the case for middle class users who often get their narcotics from friends or trusted suppliers and then take them in the safety of their own home.

“In previous years, use fell because the quality of the drugs was poor, but recently the purity of cocaine and the strength of ecstasy has improved has improved, so well off professionals, who perhaps used to take drugs in the 1990s they have returned to the marketplace.”

Almost 40 per cent of adults who took part in the survey said they believed it would be easy for them to get hold of drugs within 24 hours if they wanted them. However the figures did show that drug use amongst women had fallen to its lowest level in more than 20-years.

A new report provides insight into how traffickers move cocaine to the lucrative European market, including the key trafficking routes and smuggling techniques criminal groups have adopted to skirt drug interdiction efforts.

The recently released 2016 EU Drug Trafficking Report by the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) and Europol explains Latin America’s role in the European cocaine industry, and the different routes and methods used to traffic the drug across the Atlantic (see map below).

Colombia, Brazil and Venezuela are singled out as “key departure points” for Europe-bound cocaine, from where the drug is smuggled out in vessels, private yachts or by air, among other methods.

According to the report, the increasing importance of Brazil suggests that Bolivia and Peru are expanding their role as suppliers for the European market. The traffic of Colombian cocaine into Venezuela across a “porous border” has similarly increased. From Venezuela, criminal groups use both flights and maritime routes — capitalizing on the busy traffic off the Venezuelan coast — to send the drugs to Europe.

Despite data from the United Nations Office on Drugs and Crime (UNODC) suggesting otherwise, the report adds, Colombia is likely to continue being a key shipment point for cocaine heading to Europe, as evidenced by its growing production figures and continuing seizures. Ecuador and Argentina are also mentioned as departure points for the drug.

The Caribbean and West Africa are reportedly the two most common transit zones for cocaine moving across the Atlantic, and Central America appears to be becoming an increasingly important stop-off point. The Caribbean Sea’s main trafficking hubs are the Dominican Republic and Jamaica, although there have been reports that some activity has shifted to Caribbean countries further east.

Central America and the Caribbean was the only area to see a rise in cocaine seizures in 2013, with confiscations nearly doubling to 162 metric tons from 78 metric tons a year earlier, according to the EMCDDA. Behind the increase was a 800 percent spike in Dominican Republic seizures, which reached 86 metric tons in 2015. The apparent escalation of illegal trafficking through the Caribbean is described as a possible result of recent crackdowns in Mexico and Central America.

West Africa’s Bight of Benin — between Ghana and Nigeria — as well as the islands of Cape Verde, Madeira and the Canary Islands, make up the second major transit zone for cocaine heading to Europe. Nevertheless, the report points out that the Bight of Benin may be have lost importance in recent years.

Once on the other side of the Atlantic, cocaine continues its journey by sea, land or air, principally to western or southern Europe. In 2014, Spain, Belgium, the Netherlands, France and Italy reportedly accounted for 80 percent of the 61.6 metic tons of cocaine seized in the European Union.

The largest ports on the continent — Rotterdam in Holland, and Antwerp, Belgium — are thought to be key entry points for cocaine. Dutch police estimated that 25 to 50 percent of all cocaine filtered into Europe through Rotterdam, following the seizure of 10 metric tons of the drug at the port in 2013. Of the 11 million containers that pass through the Rotterdam annually, only 50,000 are scanned (0.45 percent). Other key entry ports are Algeciras and Valencia in Spain, and Hamburg in Germany.

The EMCDDA expressed increasing concern over the use of existing trafficking routes for other drugs to move cocaine, including cannabis corridors in Morocco and Algeria and heroin corridors in Tanzania. The report warns that Tanzania may emerge as a new cocaine route to Europe, given an increase in seizures in East Africa and as a consequence of the Panama Canal’s expansion.

The vast capacity for moving drugs and diversity of routes offered by maritime transport makes it the preferred option for cocaine traffickers to Europe. Traffickers are increasingly hiding cocaine in shipping containers aboard commercial vessels, which makes it harder to detect. Seizures involving containers have reportedly gone up sixfold since 2006.

Colombian and Italian organized crime networks reportedly continue to dominate the cocaine trade in Europe, in cooperation with Dutch, British, Spanish and Nigerian groups. The Netherlands and Spain are primary distribution centers.

InSight Crime Analysis

One of the most interesting trends highlighted by the report is that traffickers prefer to transit through the Caribbean rather than Central America on their way to Europe. While this may appear to be the easiest route, in the past organizations were known to send drugs to Central American countries before crossing the Atlantic.

The theory that the Caribbean is re-emerging as a popular drug route as Central American traffic declines has been suggested since at least 2010, and evidence over the years has both supported and refuted this theory.

There is a general consensus that tougher interdiction in Central America and Mexico is behind the supposed revival of the Caribbean corridor that had been popular in the 1980s, although such predictions have mainly be applied to drug trafficking to the United States. Still, it appears that the Caribbean route is more significant for Europe-bound cargo, as Central America remains the main trafficking corridor for northbound narcotics.

Another revealing takeaway from the report is the evolution of trafficking techniques used by criminals to skirt interdiction efforts.

The growing use of shipping containers to move cocaine demonstrates how criminal organizations are taking advantage of increasing global maritime traffic to run their business. Part of this trend is the increasingly popular “rip-on/rip-off” technique, which relies on the use of corrupt port officials to slip drugs into legitimate containers by breaking and replacing the security seal at the point of origin. Concealing cocaine with perishable goods also ensures the drugs pass through controls faster.

It is unsurprising that traffickers should take advantage of shipping routes — maritime trade handles tremendous volume and is a sector often overlooked in the fight against organized crime, providing the perfect cover for drug smugglers.

In addition, corruption, informality and a lack of resources in many departure ports makes it easier for groups to smuggle their drugs onto ships. Such is the case in Peru, where Mexican traffickers reportedly control Pacific drug routes to Europe.

The report illustrates how criminal groups must be consistently creative to survive, noting new smuggling techniques used by drug mules that include ingesting liquid rather than powder cocaine, and concealing drugs in breast implants.

Europe’s relevance to the global cocaine trade is not to be underestimated. High profit margins for traffickers and a saturated US market are likely to increase its importance in the coming years.

A study of mice found that the drug can trigger out-of-control “autophagy”, a process by which cells digest themselves.

When it is properly regulated, autophagy provides a valuable clean-up service – getting rid of unwanted debris that is dissolved away by enzymes within cell “pockets”.

Dr Prasun Guha, from Johns Hopkins University School of Medicine in the US, who led the research published in the journal Proceedings of the National Academy of Sciences, said: “A cell is like a household that is constantly generating trash. Autophagy is the housekeeper that takes out the trash – it’s usually a good thing. But cocaine makes the housekeeper throw away really important things, like mitochondria, which produce energy for the cell.”

The scientists carried out post mortems that showed clear signs of autophagy-induced cell death in the brains of mice given high doses of cocaine. They also found evidence of autophagy in the brain cells of mice whose mothers received the drug while pregnant.

The scientists showed that an experimental drug called CGP3466B was able to protect mouse nerve cells from cocaine death due to autophagy. Since the drug has already been tested in clinical trials to treat Parkinson’s and motor neurone disease, it is known to be safe in humans. But much more research is needed to find out whether the drug can prevent the harmful effects of cocaine in people, said the team.

Co-author Dr Maged Harraz said: “Since cocaine works exclusively to modulate autophagy versus other cell death programs, there’s a better chance that we can develop new targeted therapeutics to suppress its toxicity.”

In Brazil, crack cocaine use remains a healthcare challenge due to the rapid onset of its pleasurable effects, its ability to induce craving and addiction, and the fact that it is easily accessible. Delayed action on the part of the Brazilian Government in addressing the drug problem has led users to develop their own strategies for surviving the effects of crack cocaine use, particularly the drug craving and psychosis. In this context, users have sought the benefits of combining crack cocaine with marijuana. Our aim was to identify the reasons why users combine crack cocaine with marijuana and the health implications of doing so.

METHODS:

The present study is a qualitative study, using in-depth interviews and criteria-based sampling, following 27 crack cocaine users who combined its use with marijuana. Participants were recruited using the snowball sampling technique, and the point of theoretical saturation was used to define the sample size. Data were analyzed using the content analysis technique.

RESULTS:

The interviewees reported that the combination of crack cocaine use with marijuana provided “protection” (reduced undesirable effects, improved sleep and appetite, reduced craving for crack cocaine, and allowed the patients to recover some quality of life).

CONCLUSIONS:

Combined use of cannabis as a strategy to reduce the effects of crack exhibited several significant advantages, particularly an improved quality of life, which “protected” users from the violence typical of the crack culture. Crack use is considered a serious public health problem in Brazil, and there are few solution strategies. Within that limited context, the combination of cannabis and crack deserves more thorough clinical investigation to assess its potential use as a strategy to reduce the damage associated with crack use.

It’s called Shatter and it looks like dark-amber toffee. It’s THC, the chemical that causes the high in marijuana, extracted from the plant and has highly addictive qualities, said Stratford police Insp. Sam Theocharis.

It’s been around for a while but it’s new to Stratford, Theocharis said. Police have started to see the drug a bit more frequently and wanted to get the message out to the public.

“When you look at it, it just looks like goo but it’s a new form of marijuana drug,” he said.

Shatter is clear, smooth and solid. It can consist of more than 80% THC, according to the High Times website.

Police seized some Tuesday along with methamphetamine, cocaine, marijuana and prescription drugs after an investigation by the Street Crime Unit. Two men in their 40s were arrested and face several charges including possession for the purpose of trafficking. The drugs seized are valued at more than $1,500. Cell phones, scales and baggies were also seized, police said.

Shatter sells for about $100 a gram on the streets. It’s dangerous and often leads to overdose, police said. Whether it will overshadow crystal meth and oxycodone in popularity has yet to be seen.

“I can’t predict but anything that gives you a better high is going to be sought after,” Theocharis said.

President Obama this week told an audience in Jamaica that U.S. efforts against illegal drugs were “counterproductive” because they relied too much on incarceration—particularly for “young people who did not engage in violence.”

In what the president termed “an experiment … to legalize marijuana” in Colorado and Washington state, he said he believed they must “show that they are not suddenly a magnet for additional crime, that they have a strong enough public health infrastructure to push against the potential of increased addiction.”

In regard to Jamaica and the entire Caribbean and Central American region, he said, “a lot of folks think … if we just legalize marijuana, then it’ll reduce the money flowing into the transnational drug trade, there are more revenues and jobs created.”

To some of us, Jamaica hardly seems an auspicious location for encouraging “experimentation” with drugs, in particular because of the challenges already faced by their deficient institutions of public health and criminal justice. The U.S. Department of State 2015 International Narcotics Control Strategy Report(INCSR) states:

Jamaica remains the largest Caribbean supplier of marijuana to the United States and local Caribbean islands. Although cocaine and synthetic drugs are not produced locally, Jamaica is a transit point for drugs trafficked from South America to North America and other international markets. In 2014, drug production and trafficking were enabled and accompanied by organized crime, domestic and international gang activity, and police and government corruption. Illicit drugs are also a means of exchange for illegally-trafficked firearms entering the country, exacerbating Jamaica’s security situation.

Drugs flow from and through Jamaica by maritime conveyance, air freight, human couriers, and to a limited degree by private aircraft. Marijuana and cocaine are trafficked from and through Jamaica into the United States, Canada, the United Kingdom, Belgium, Germany, the Netherlands, and other Caribbean nations. Jamaica is emerging as a transit point for cocaine leaving Central America and destined for the United States, and some drug trafficking organizations exchange Jamaican marijuana for cocaine. . . .

The conviction rate for murder was approximately five percent, and the courts continued to be plagued with a culture of trial postponements and delay. This lack of efficacy within the criminal courts contributed to impunity for many of the worst criminal offenders and gangs, an abnormally high rate of violent crimes, lack of cooperation by witnesses and potential jurors, frustration among police officers and the public, a significant social cost and drain on the economy, and a disincentive for tourism and international investment.

This does not seem like a place where “legal” marijuana would contribute to “reduced money flow” to the transnational drug trade, or “create jobs.” The president apparently thinks Jamaica should consider allowing more drugs, based on a faulty understanding of what is actually happening in Jamaica and in the U.S.

His charge of high incarceration rates for non-violent offenders is not factual. For instance, data show that only a fraction of one percent of state prison inmates are low-level marijuana possession offenders, while arrests for marijuana and cocaine/heroin possession and use were no more than 7 percent of all arrests,nationwide, in 2013.

Though critics of drug laws claim that hundreds or even thousands of prisoners are low-level non-violent offenders unjustly sentenced, the reality was shown recently by the President’s inability to find more than a handful of incarcerated drug offenders who would be eligible for commutation of their sentence because they fit the mythological portrait of excessive or unjust drug sentences.

As for Central America, Obama’s policies have shown stunning neglect. Actual aid for counter-drug activities, and for resources for interdicting smugglers have all diminished, while the countries of Central America have become battlegrounds for Mexican cartels, with meth precursors piling up at the docks, the cocaine transiting Venezuela to Honduras is surging, and violence is at an all-time high, with families fleeing north in unprecedented numbers. The Caribbean/Central American region has become deeply threatened, as noted by the State Department report above—torn apart by drug crime.

In this context the president encourages governments in the region to make drugs more acceptable and more accessible in their communities, and with even greater legal impunity?

Moreover, these developments have been accompanied by a steady drumbeat of medical science reports increasingly showing the serious dangers of marijuana use, especially for youth. Yet President Obama speaks in a manner increasingly disconnected from the domestic and international reality of the drug problem.

Source: David W. Murray and John P. Walters WEEKLY STANDARD April 11, 2015

The largest recent US national survey of drink and drug problems shows that outside the addiction treatment clinic, remission is the norm and recovery common. After 14 years half the people at some time dependent on alcohol were in remission, a milestone reached for cannabis after six years, and for cocaine after just five.

SUMMARY Among the US general adult population, and for each of nicotine, alcohol, cannabis and cocaine (including crack), this study sought to estimate the time from onset of dependence to remission, the cumulative probability of remission in different racial/ethnic groups, and to identify factors related to the probability of remission.

It drew its data from the National Epidemiological Survey of Alcohol and Related Conditions (NESARC) conducted in 2000–2001, which focused on drinking disorders but also asked about other forms of drug use and psychological problems. The aim was to interview a representative sample of civilian, non-institutionalised adults aged 18 and over living in households and group residences such as college halls, boarding houses and non-transient hotels. About 8 in 10 of the sample responded to the survey yielding 43,093 respondents. The featured report investigated the subgroups who had some time in their lives been dependent on nicotine (of which there were 6937), alcohol (4781), cannabis (530) or cocaine (408).

Dependence was defined as meeting the dependence criteriaof the applicable version of the American Psychiatric Association’s DSM manual, DSM-IV. ‘Lifetime’ dependence was diagnosed if the respondent reported having experienced at least three specific signsof this syndrome within the same 12-month period at some point in their life. The age this first happened for any particular substance was the onset year, while the remission year was based on the age when the respondent’s answers indicatedthey had last stopped meeting dependence criteria for the drug, and had continued to do so for at least a year until interviewed for the survey – essentially, the most recent (at least so far) lastinglysuccessfulremission. It was on this basis that the study calculated remission rates for individual substances and related them to the time between the onset of dependence and remission.

Main findings

Proportion of dependent users in remission

Within a year of first becoming dependent, 3% each of smokers and drinkers were in remission and remained so until they were surveyed. For cannabis the figure was nearly 5% and for cocaine, nearly 9%. After ten years the proportions in remission had risen to 18% for nicotine, 37% for alcohol, 66% for cannabis and 76% for cocaine chart. It could be estimated that by the end of their lives 84% of formerly dependent smokers would be in remission, 91% for alcohol, 97% for cannabis and 99% for cocaine. About 26 years after first becoming dependent, half the people at some time dependent on nicotine were in remission, a milestone reached for alcohol after 14 years, for cannabis six years, and for cocaine five years.

Once other factors had been taken in to account, for each of the substances, men who had been dependent at some time were significantly less likely than women to be in remission, especially in respect of the two illegal drugs, cannabis and cocaine; for every 10 women only about six men were in remission from dependence on these drugs. Black Americans once dependent on nicotine or cocaine were less likely to be in remission than white Americans – for cocaine, half as likely. After four years, about 50% of whites had sustained remission from dependence on cocaine; African Americans took nine years to reach the same milestone.

About 80% of people at some time dependent on nicotine or alcohol and almost all those once dependent on cannabis or cocaine had also at some time met diagnostic criteria for another psychiatric disorder, including conduct (antisocial behaviour in early life) and personality disorders. Once other factors had been taken in to account, people who had met criteria for conduct disorder were much more likely than others to have overcome their dependence on cannabis. In contrast, a diagnosis of a personality disorder was associated with a lower probability of remission from cannabis (and also alcohol) dependence. Having once experienced mood and anxiety disorders was unrelated to remission from dependence on any of the four substances.

The authors’ conclusions

The general picture is that the vast majority of people in the USA once dependent on nicotine, alcohol, cannabis or cocaine stop being dependent at some point in their lives, and this happens after fewer years for cannabis or cocaine than for nicotine or alcohol. Black Americans stay dependent longer on nicotine and cocaine than white Americans, and probabilities of remission are associated with social and psychological characteristics and dependence on other substances. However, the fact that that many people once dependent were no longer at the time of the survey should be interpreted with caution given the irregular course of addictions punctuated by remissions and relapses; their remission may have been temporary. Possible explanations for these findings are considered below.

More than two thirds of remissions from cannabis and cocaine dependence occurred within the first decade after onset of dependence, but only a fifth for nicotine and a third for alcohol. These differences may be explained in part by how quickly adverse physical, psychological and social consequences become apparent. For instance, the risk of early cardiovascular problems is much higher among individuals dependent on cocaine than among those dependent on nicotine or alcohol. Behavioural disturbances resulting from cannabis or cocaine dependence and their illegal status impose stronger social pressures to remit. The pervasive availability of alcohol and nicotine also means pervasive environmental prompts to using the drugs. Particularly for nicotine, perceived immediate benefits including anxiety and stress reduction, improved cognitive performance, and weight control, may initially outweigh perceived potential harms from long-term use.

Consistent with previous studies, black Americans once dependent on cocaine were less likely to remit than their white counterparts. Psychosocial factors that commonly affect black populations, including discrimination and lower levels of social capital, have been recognised as barriers to remission and triggers to use or relapse; genetic factors may also contribute.

Men were less likely than women to remit from dependence, perhaps because substance use is more damaging (physically, mentally and socially) for women, heightening motivation to stop using. Feelings of guilt and concerns about substance use during pregnancy and child-rearing may also play a particular part in prompting remission among women.

Individuals who met criteria for a personality disorder were less likely to remit from alcohol or cannabis dependence. This may be because characteristics of these disorders such as being impulsive, intolerant to stress, anxious, and craving new experiences, also predispose to substance use, and these characteristics tend to persist.

Among the limitations of the study were that it omitted institutionalised individuals including prisoners. People whose substance use led to their early death would also have been missed, as may some with severe but non-fatal consequences. These omissions may have caused an overestimation of the probability of remission across the entire population. The study also had no information on the number and duration of remission episodes over an individual’s lifetime; it could only relate other factors to the latest of these remissions.

COMMENTARY The good news from this analysis is that, in the US context, rather than continued dependence, remission is the norm. Most people overcome or grow out of their dependence on the drugs analysed by the study – for cocaine and cannabis, after just five or six years, and for alcohol, after 14, and over their lives people continue to remit until nearly all are no longer dependent. But at least in respect of drinking, there are a set of multiply problematic drinkers who despite treatment, take many more years to stop being dependent. The findings on black versus white Americans suggest that remission rates depend on socioeconomic factors; sampled at another period in the USA’s economic cycles or in respect of drugs used predominantly by more or less advantaged sections of the population, remission rates too might differ, and look more or less like the chronic disease model.

The data presented in the featured article did not show whether the user ‘in remission’ had simply become dependent on another drug. Within the set of illegal drugs and medicines, this seemed uncommon, because the total remission rate was so high. But it seems more than possible that some who matured out of illegal drug use instead took up heavy drinking, in social and legal terms, a dependence easier to live with as an adult.

Remission rates looking forward

An acknowledged weakness of the featured report is that it asked respondents to recall changes which may have happened many years ago. However, the survey was repeated about three years later when 87% of the people who still qualified for the survey were re-interviewed. The follow-up offered an opportunity to see how many dependent at the time of the first survey had recovered three years later. These analyses seem only to have been done for drinking, for which they confirm that most people cease to be dependent though most too continue to experience drink-related problems and to sometimes drink heavily, and remain vulnerable to relapse. This average impression results from the pooling of dramatically different trajectories, from older multiply problematic alcoholics who usually do not remit despite treatment, to youngsters who generally quickly remit without formal help. Details below.

Among the re-interviewed sample were 1172 of the 1484 people who had been dependent on alcohol in the year before the first interview three years before. Nearly two thirds were longer dependent in the year before the follow-up interview. So complete was their recovery that a fifth of those previously dependent had in the past year experienced no indications of abuse or dependence; of these, three quarters were still drinking. About 11% not only had no symptoms, but were exclusively drinking within low-risk guidelines, evenly split between those drinking moderately and those not drinking at all.

But this broad-brush picture hid substantial variation in the fates of different types of dependent drinkers. At one extreme were the most severely affected drinkers with multiple psychological problems and on average about nine years of dependence behind them, two thirds of whom were still dependent at the second interview. At the other were young adults and older drinkers with few complicating psychological disorders and few years of dependent drinking. For most of these the dip in to dependence was a phase which (at least for time being) was over by the the second interview, when just under 30% were still dependent.

At least for the three years between the surveys, remission was very stable. Among the re-interviewed sample were 1772 of the 2109 who three years before had been in “full remission” from past dependence on alcohol, meaning that even though they may sometimes have drunk above low-risk guidelines, for the past 12 months they had reported no symptoms of alcohol abuse or dependence. Of these just 5% had slipped back to being dependent in the year before the second interview, though a third who had been drinking above low-risk guidelines had re-experienced some symptoms of alcohol abuse or dependence. Most stable in their recovery were the abstainers, of whom just 1 in 50 experienced such symptoms. The much greater stability of recovery in abstainers and low-risk drinkers was confirmed when other factors had been taken in to account, but was not apparent among the younger adults in the sample.

Treatment’s impact

Few dependent drug users recover through treatment and fewer still dependent on alcohol – in theNESARC survey on which the featured analysis was based, of those no longer dependent on alcohol,just 24%had at any time been in any kind of treatment for their drinking problems. Over two thirds of those who achieved more complete forms of recovery also did so without treatment.

While this shows that in the USA, treatment is generally not needed to recover from substance dependence, treatment may still make recovery more likely. In respect of dependence on alcohol, one analysis of data from the NESARC survey was consistent with formal treatment promoting recovery characterised by abstinence or low-risk drinking and no symptoms of abuse or dependence, but another and perhaps more reliable analysis found no such association.

Both however found that when treatment had been accompanied by attendance at 12-step mutual aid groups, recovery was more likely – especially abstinent recovery. These analyses could not however disentangle the possible effects of the motivation and conditions which drive someone to seek help, from the effect of actually receiving that help. Complicating the picture is the fact in this survey, the most severely affected and multiply comorbid drinkers with many years of dependence behind them were far more likely to seek treatment than less severely affected types of dependent drinkers. Despite seeking help, they were by a large margin the ones most likely to still be dependent when the survey was repeated three years later.

What about heroin and other opiates?

A notable omission from the illicit drugs included in the featured report was heroin and other opiates. Fortunately these were the subject of the greatest number of relevant studies in another review of follow-up studies of remission from dependence on amphetamine, cannabis, cocaine or opiate-type drugs. It included only studies of general populations or people who entered treatment in the normal way rather than enrolling in treatment trials.

Across the ten studies relevant to opiate-type drugs, every year on average between 22% and 9% of people were either abstinent or no longer dependent; the higher figure is the average of the proportions remitted among people who could be followed up, while the lower estimate includes cases who could not be followed and assumes they are still dependent. Generally the subjects were patients in treatment. Based mainly on patients in treatment, corresponding figures for cocaine were between 14% and 5%. The single study (from the USA) of a general population sample of cocaine-dependent people found that 39% had remitted four years after initially surveyed. For cannabis, the estimate was 17% per annum based on general population surveys and assuming people not followed up were still dependent.

In accordance with the featured article, such figures imply that within 10 years most dependent users of these drugs will no longer be dependent and may have entirely ceased use.

Racial differences reflect socioeconomic status

An analysis of data from the NESARC survey showed that taking alcohol and other drugs together, the longer dependence careers of black versus white Americans was associated with their having less social and socioeconomic resources, signified by fewer being married and fewer having completed their schooling. Once these were taken in to account, racial differences were no longer significant. The implication is that it is not race as such which makes the difference, but the position black people tend to occupy in US society. Given the same disadvantages, white Americans has dependence careers just as extended as black Americans.

Diagnostic system affects remission rate

Much in this analysis depends on the definitions used in the survey. Specifically, the probability of remission equates to the probability that someone will for at least the past 12 months have dropped below experiencing three or more dependence symptoms together in respect of the same drug. From the same survey, it is known for alcohol that many will still be consuming heavily, experiencing symptoms of dependence such as withdrawal and compulsive use, and suffering poor physical and mental health (12). They may be remitted from their dependence, but not according to most understandings, ‘recovered’.

Had the line been drawn elsewhere, the chances of remission might have been substantially lower – for example, as commonly in NESARC reports on drinking (1234), if remission had been defined as non-problem moderate use or abstinence.

The latest version of the DSM manual (DSM-5) softens this binary system by diagnosing a substance use disorder when at least two symptoms are present in the same 12 months, and rating this as moderate if there were two or three, severe if four or more. ‘Abuse’ and ‘dependence’ are now subsumed within this continuum. The change seems likely to bring many more less severely affected people under the same substance use disorder umbrella as the three-symptom population investigated by the featured analysis. Their remission rates too may differ.

It is also theoretically possible that ‘remission’ may partly reflect the lack of noticeable change or struggle as with the years dependence becomes more deeply embedded and dominant in one’s life, and the change processes probed by some diagnostic questions cease to be live issues – not a sign of recovery, but of the lack such a prospect and the narrowing of life to substance use. For example, having plateaued in their use levels, long-term dependent users may no longer (or not for the past 12 months) have found themselves needing to take more of the drug to feel the desired effects, or taking more than they intended. Perhaps too in the past they had tried unsuccessfully to stop using, or had at least persistently wanted to, but now no longer tried or even wanted to. Ensuring a steady supply of drink or drugs they made no attempt to interrupt would minimise experience of withdrawal. They may also have no important interests and activities left to sacrifice to their dependence – all among the symptoms used to diagnose dependence.

Some findings from NESARC are consistent with this possibility. In the three years between the first interview and the re-interview, the alcohol dependence symptoms which fell away most often and most consistently across different types of drinkers were “taking alcohol often in larger amounts or over a longer period than was intended”, “a persistent desire or unsuccessful efforts to cut down or control use”, and withdrawal.

Similarly, young adult dependent drinkers tend not to endorse the dependence symptom relating to inability to stop drinking or cut back, presumably because they have yet to try.

Related analyses

This data from the featured report has been reanalysed to show that for each of these drugs, the probability that someone would have ceased being dependent remained the sameno matter how long ago they had first become dependent. For the author this falsified theories which assume that the longer it lasts, the deeper dependence becomes embedded in neural circuits or lifestyles.

The survey on which the featured article was based and other US national surveys were among those included in a synthesisof hundreds of studies of remission and recovery from substance use problems. This too concluded that “Recovery is not an aberration achieved by a small and morally enlightened minority of addicted people. If there is a natural developmental momentum within the course of [these] problems, it is toward remission and recovery”.

The polarized legalization debate leads to exaggerated claims and denials about pot’s potential harms. The truth lies in between.

Pretty much everyone who has spent time smoking marijuana knows at least one diehard stoner. The guy whose eyes are always red, the girl who doesn’t use the term “wake and bake” ironically, the person who just can’t seem to ever get it together. These heavy smokers might work at a low-level job or they may be unemployed—but everyone who knows them well knows that they are capable of much more, if only they had any ambition.

Is this really addiction? I believe that it is (and I don’t think that’s an argument against legalization). In fact, the reasons why marijuana is addictive elucidate the true nature of addiction itself. Addiction is a relationship between a person and a substance or activity; addictiveness is not a simple matter of a drug “hijacking the brain.” In fact, with all potentially addictive experiences, only a minority of those who try them get hooked—and people can even become addicted to apparently “nonaddictive” things, like carrots. Addiction depends on learning, context and psychology, not just neurotransmitters.

With two states having already legalized recreational marijuana use and several more considering doing so, understanding the nature of addiction is more important than ever. Partisans on both sides of the debate have made extreme claims here; some legalizers saying there’s no such thing as marijuana addiction, while some prohibitionists claim “cannabis as addictive as heroin.”

Our concepts of addiction, however, come primarily from cultural experience with alcohol, heroin and, later, cocaine. No one has ever argued that opioids like heroin don’t have the potential to cause addiction because the withdrawal symptoms—vomiting, shaking, pallor, sweating and diarrhea—are objectively measurable. Opioids cause physical dependence that is evident when they become unavailable. The same is true for alcohol, where withdrawal is even more severe and can sometimes even be deadly.

So early researchers focused on these measurable symptoms related to alcoholism and opioid addictions in defining addiction: Using a drug could lead to becoming tolerant to it, tolerance could lead to dose escalation, which could in turn lead to physical dependence, and then the addiction could be driven by the need to avoid the painful symptoms of withdrawal. It was simple and physical.

In this view, however, cocaine and marijuana were not “really” addictive. While people can experience withdrawal symptoms like irritability, depression, craving and sleep problems when quitting these drugs, these are much more subjective and therefore can be dismissed as “psychological” rather than physical. You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

And since most of us like to believe that we have much more control over our minds than we do over physical symptoms, “psychological” addiction is seen as far less serious than the “physical” type. It’s the remnants of this kind of thinking that mainly underlie the idea that marijuana addiction doesn’t exist. Unfortunately, that view of addiction is stuck in the 1970s.

In the 1980s—ironically, not long after Scientific American caused a big controversy by arguing that snorted cocaine is no more addictive than eating potato chips—entrepreneurs began marketing a ready-made smokeable form of the drug. The birth of crack shattered the idea that “physical” dependence is more serious than psychological dependence because people with cocaine addictions don’t vomit or have diarrhea when they quit; while they may appear desperate, it’s not in the physically obvious way of heroin or alcohol withdrawal. And so, if you are going to argue that marijuana is not addictive because you don’t get sick when you quit, you also have to argue the same for crack.

In the 1970s view, cocaine and marijuana were not “really” addictive: You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

Good luck with that one, I say. Clearly, crack-addicted people are every bit as compulsive as those with heroin problems—and their criminal involvement if they can’t afford the drug is at least equally likely, though not as common as has been claimed. Crack dealt a deathblow to the “psychological” vs. “physical” distinction—and if it hadn’t, neuroscience was creeping up to show that the psychological and the physical aren’t exactly distinct anyway.

In the ‘70s and ‘80s, researchers also began recognizing that simply detoxing heroin addicts—getting them through the two-week period of intense physical withdrawal symptoms—is not effective treatment. If heroin addiction was driven primarily by the need to avoid withdrawal, addicted people should be out of the woods after they complete cold turkey. But as those of us who have been through it know, that is far from the hardest part.

While kicking heroin isn’t fun, staying off it in the long run is the problem—those “mere” psychological cravings are what drive addiction. Physical dependence isn’t the main problem; it isn’t even necessary. Indeed, we now know that you can actually have physical dependence without any addiction at all: There are some blood pressure medications, for example, that can have deadly withdrawal symptoms if not tapered properly, but people on these meds don’t crave them even though they are quite dependent. Similarly, antidepressants like Paxil have physical withdrawal symptoms, but because they don’t produce a high, you don’t see people robbing drug stores to get them.

So what is addiction, then, if tolerance, withdrawal and physical dependence aren’t essential to it? All of these facts point to one definition that can sum up the problem: Addiction is compulsive use of a substance or engagement in a behavior despite negative consequences. (Put more in neuroscience, addiction is a learned distortion in the brain’s motivational systems that make us persist in pursuing things linked to evolutionary fitness like food and sex.) Anything that causes pleasure via these systems—and that’s basically anything that is possible to enjoy—can be addictive to some person at some time. And that includes marijuana (and, for that matter potato chips).

This doesn’t mean that marijuana addiction is necessarily as severe as cocaine, heroin or alcohol addiction—in fact, it typically isn’t. If given the choice, most families would vociferously prefer having a member addicted to marijuana rather than to cocaine, heroin or alcohol. The negative consequences associated with marijuana addiction tend to be subtler: lost promotions, for example, rather than lostjobs; worse relationships, not no relationships. And of course, no risk of overdose death.

Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities.

But this is also what can make it insidious. Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities. With any pattern of regular drug use, it’s important to continually track whether the risks outweigh the benefits, keeping in mind that addiction itself may distort this calculation. This is especially true with marijuana.

However, as with all other drugs, only a minority of marijuana users ever struggle with addiction. Research suggests that about 10% get hooked—and on average, marijuana addiction lasts six years. Even more than other addictions, marijuana addiction seems to be driven by self-medication of mental health problems—90% of people with marijuana addiction also have another addiction or mental illness, typically alcoholism or antisocial personality disorder.

This suggests that exposing more of the population to marijuana won’t necessarily increase the addicted population. First, people with antisocial personality disorder, by definition, tend not to be law abiding, so most have probably already tried it. Second, the percent of people with other pre-existing mental illness will not change because marijuana becomes legal—in fact, in the UK, when they reversed their prior liberalization of marijuana law because of fears related to increased schizophrenia, psychosis rates actually went up. (The link probably wasn’t causal, but it does suggest that legal crackdowns on cannabis don’t prevent related psychosis).

If some people with alcohol, cocaine or heroin addiction switch to marijuana instead, overall harm would be reduced. As I and others have been reporting at least since 2001, using marijuana as an “exit” drug is a real phenomenon, both in cocaine and opioid addiction.

When we consider the risks of various substances, we tend to do so in isolation—but that’s not how choices are made in the real world. Most people would rather their partners have no addictions—but again, some are clearly worse than others. Marijuana craving is rarely as severe as crack craving, as is obvious.

Still, like anything that can be pleasurable, marijuana can be addictive. This doesn’t mean all addictions are the same or that it is as addictive as the currently legal drugs alcohol and tobacco—the data shows it is less so.

Pretending it can’t do any harm at all, however—or that there aren’t people who are addicted to it—does no one any good. If we want better drug policy, as with other types of recovery, we need to avoid denial.

Cocaine addicted individuals may continue their habit despite unfavorable consequences like imprisonment or loss of relationships because their brain circuits responsible for predicting emotional loss are impaired, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published today in The Journal of Neuroscience.

The study focuses on the difference between a likely reward (or loss) related to a given behavior and a person’s ability to predict that outcome, a measurement known as Reward Prediction Error, or RPE. Such RPE signaling is believed to drive learning in humans, which guides future behavior. After learning from an experience, we can, in the best case, change our behavior without having to go through it again, and thus maximize rewards and avert expected losses. Past research has determined that prediction of actual reward or loss is managed by shifting levels of the nerve signaling chemical dopamine produced by nerve cells in the midbrain, where changes in dopamine levels accompany unexpected gains and losses.

The Mount Sinai study recorded the brain activity of 75 subjects (50 cocaine users and 25 healthy controls) using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game. Each person had to predict whether or not they would win or lose money on each trial.

Results showed that the group of the 50 cocaine users had impaired loss prediction signaling, meaning they failed to trigger RPE signals in response to worse-than-expected outcomes compared to the 25 healthy people comprising the control group. The results offer insights into the compromised ability of addicted individuals to learn from unfavorable outcomes, potentially resulting in continued drug use and relapse, even after encountering numerous losses.

“We found that people who were addicted to cocaine have impaired loss prediction signaling in the brain,” said Muhammad Parvaz, PhD, Assistant Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai and the lead author of the study. “This study shows that individuals with substance use disorder have difficulty computing the difference between expected versus unexpected outcomes, which is critical for learning and future decision making. This impairment might underlie disadvantageous decision making in these individuals.”

Next, the study looked at individual differences among the 50 cocaine users. Half of the subjects had used cocaine within 72 hours of the study and the other half had abstained for at least 72 hours. The cocaine addicted individuals with the more recent use had higher electrical activity associated with the brain’s reward circuit when they had an unpredicted compared to a predicted win, a pattern that was similar to the 25 healthy controls. The cocaine users who had abstained for at least 72 hours did not show this higher activity in response to an unpredicted win. These findings are consistent with the hypothesis that in addiction the drug is taken to normalize a certain brain function, which in this case is RPE signaling of better-than-expected outcomes.

“This is the first time a study has targeted the prediction of both gains and losses in drug addiction, showing that deficits in prediction error signaling in cocaine addicted individuals are modulated by recent cocaine use,” said principal investigator Rita Goldstein, PhD, Chief of Neuropsychoimaging of Addiction and Related Conditions, Chief of the Brain Imaging Center, and Professor of Psychiatry and Neuroscience at the Icahn School of Medicine. “Direction of results supports the self-medication hypothesis in drug addiction whereby drug self-administration improves response to reward in drug addicted individuals. The reductions in prediction of loss across all cocaine addicted individuals included in this study are also of great interest; they could become important markers that can be used to predict susceptibility for addiction or relapse or to develop targeted interventions to improve outcome in this devastating, chronically relapsing disorder.”

Cocaine addicts can’t recognise loss – such as the consequences of a break-up or being sent to jail – because the drug changes their brain, according to a new study.

Researchers found cocaine addicts may continue their destructive drug habit despite such huge personal setbacks because their brain circuits responsible for predicting emotional loss are impaired. They say the find could be used to develop new treatments, and spot those most at risk of relapsing.

Cocaine

The new study recorded the brain activity of 75 people – 50 cocaine users and 25 healthy controls – using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game. Each person had to predict whether or not they would win or lose money on each trial.

The study, published in The Journal of Neuroscience, focuses on the difference between a likely reward, or loss, related to a given behaviour and a person’s ability to predict that outcome – a measurement known as Reward Prediction Error, or RPE.Such RPE signalling is believed to drive learning in humans, which guides future behaviour. After learning from an experience, we can, in the best case, change our behaviour without having to go through it again.

Previous research determined that predictions of actual reward or loss are managed by shifting levels of the nerve signaling chemical dopamine produced by nerve cells in the brain, where changes in dopamine levels accompany unexpected gains and losses.The new study recorded the brain activity of 75 people – 50 cocaine users and 25 healthy controls – using EEG, a test that detects electrical activity in the brain, while subjects played a gambling game. Each person had to predict whether or not they would win or lose money on each trial.

Results showed that the group of cocaine users had impaired loss prediction signaling, meaning they failed to trigger RPE signals in response to worse-than-expected outcomes compared to the 25 healthy people.

Researchers say their findings offer insights into the compromised ability of addicts to learn from unfavourable outcomes, potentially resulting in continued drug use and relapse, even after suffering major losses.

Study lead author Doctor Muhammad Parvaz, Assistant Professor of Psychiatry at the Icahn School of Medicine in the US, said: ‘We found that people who were addicted to cocaine have impaired loss prediction signalling in the brain.

‘This study shows that individuals with substance use disorder have difficulty computing the difference between expected versus unexpected outcomes, which is critical for learning and future decision making.

‘This impairment might underlie disadvantageous decision making in these individuals.’

Half had used cocaine within 72 hours of the study and the other half had abstained for at least 72 hours.

The cocaine addicts with the more recent use had higher electrical activity associated with the brain’s reward circuit when they had an unpredicted compared to a predicted win, a pattern that was similar to the 25 healthy controls. The cocaine users who had abstained for at least 72 hours did not show the higher activity in response to an unpredicted win.

The researchers said these findings are consistent with the hypothesis that in addiction the drug is taken to normalise a certain brain function, which in this case is RPE signalling of better-than-expected outcomes. Principal investigator Doctor Rita Goldstein said: ‘This is the first time a study has targeted the prediction of both gains and losses in drug addiction, showing that deficits in prediction error signalling in cocaine addicted individuals are modulated by recent cocaine use.

‘The reductions in prediction of loss across all cocaine addicted individuals included in this study are also of great interest; they could become important markers that can be used to predict susceptibility for addiction or relapse or to develop targeted interventions to improve outcome in this devastating, chronically relapsing disorder.’

When Robin Williams committed suicide last week, his publicist announced he had been suffering from severe depression. Within days, his wife revealed he had also been diagnosed with Parkinson’s disease and was experiencing the early stages of the deadly disease.

Shocked experts and fans believed that the combination of the two ailments pushed the beloved comedian over the edge and caused him to take his own life.

For years, Williams had openly discussed his battle with depression and also with substance abuse. Board-certified neurosurgeon Dr. Russell Blaylock believes that Williams’ substance abuse — specifically his use of cocaine — was at the root of his Parkinson’s disease. In fact, a major study has found that cocaine users are at much higher risk for the brain illness.

“Robin said in interviews that he used a lot of cocaine in his youth and for many years,” Dr. Blaylock tells Newsmax Health. “Cocaine triggers excitotoxicity in the area of the brain pathological for Parkinson’s disease (PD).”

Excitotoxicity is the process by which nerve cells in the brain are damaged and killed by the excessive release of certain neurotransmitters, such as glutamate, that cause brain cells to become overexcited and die.

With PD, the brain cells that produce dopamine die, which affects the nervous system causing shaking and difficulties with balance. Some patients may have problems walking and talking. In addition, symptoms may include depression.

A 2005 study at St. Jude Children’s Research Hospital found that people who abuse cocaine increase their risk of developing Parkinson’s disease. They found that cocaine altered nerves in the substantia nigra region of the brain, making them more vulnerable to a toxin (MPTP) known to cause symptoms of PD.

Williams admitted he suffered cocaine addiction in the 70s and early 80s, but the untimely death of his friend John Belushi from a drug overdose caused him to quit using drugs and drinking. He never took cocaine again, he told the Guardian newspaper.

“I knew (cocaine) would kill me,” he said. Not only that, he didn’t enjoy the drug. “Cocaine – paranoid and impotent, what fun,” he said sarcastically. “There was no bit of me thinking, ‘Ooh, let’s go back to that.’ Useless conversations until midnight, waking up at dawn feeling like a vampire on a day pass. No.”

Still, alcohol and depression were constant battles, although his wife said he was sober at the time of his death.

However, the heavy cocaine use of his past may have already done its damage, setting up Williams to develop Parkinson’s in the future, said Dr. Blaylock.

“I have tried many times to warn foolish youth of the association of Parkinson’s with cocaine,” says Dr. Blaylock. “Cases like Robin Williams are tragic.”

So who supports decriminalising cocaine, heroin, LSD, methamphetamine, ecstasy and all dangerous drugs, including marijuana?

No, it’s not your teenage nephew. It’s President Obama’s new acting head of the Justice Department’s Civil Rights Division, Vanita Gupta. In 2012, Gupta wrote that “states should decriminalise simple possession of all drugs, particularly marijuana, and for small amounts of other drugs.” (Emphasis mine).

Last week, President Obama appointed Vanita Gupta to the position of acting head. According to the Washington Post, the administration plans to nominate her in the next few months to become the permanent assistant attorney general for the Civil Rights Division. Her views on sentencing reform – a bi-partisan effort in recent years – have earned her qualified kudos from some conservatives.

But her radical views on drug policy – including her opinion that states should decriminalise possession of all drugs (cocaine, heroin, LSD, ecstasy, marijuana and so on) should damper that support of those conservatives, and raise serious concerns on Capitol Hill.

As the deputy legal director of the American Civil Liberties Union and the director of its Center for Justice, Gupta’s legal and policy positions are well documented in her long paper trail, which, no doubt, will be closely scrutinised if and when she is nominated and gets a hearing before the Senate Judiciary Committee.

To begin, she believes that the misnamed war on drugs “is an atrocity and that it must be stopped.” She has written that the war on drugs has been a “war on communities of color” and that the “racial disparities are staggering.” As the reliably-liberal Huffington Post proclaimed, she would be one of the most liberal nominees in the Obama administration.

Throughout her career, 39-year old Gupta has focused mainly on two things related to the criminal justice system: first, what she terms Draconian “mass incarceration,” which has resulted in a “bloated” prison population, and second, the war on drugs and what she believes are its perceived failures.

She is particularly open about her support for marijuana legalisation, arguing in a recent CNN.comop-ed that the “solution is clear: …states could follow Colorado and Washington by taxing and regulating marijuana and investing saved enforcement dollars in education, substance abuse treatment, and prevention and other health care.”

Yet just last week the current Democratic Governor of Colorado, John Hickenlooper, said that legalising recreational use of marijuana was a “reckless.” And there is a growing body of evidence to prove his point: (1) pot-positive auto fatalities have gone up 100 percent in 2012, the year the state legalized pot; (2) the majority of DUI drug arrests involve marijuana and 25 to 40 percent were pot alone; (3) from 2011 through 2013 there was a 57 percent increase in marijuana-related emergency room visits – and there are many other indications of failure. New research, from a 20-year study, proves the dangers of marijuana.

But Gupta does not stop with marijuana. In calling for all drugs to be decriminalised – essentially legalising all dangerous drugs – Gupta displays a gross lack of understanding of the intrinsic dangers of these drugs when consumed in any quantity.

Heroin, LSD, ecstasy, and methanqualone are Schedule I drugs, which are defined as “the most dangerous drugs of all the drug schedules with potentially severe psychological or physical dependence.” Cocaine, methamphetamine, Demerol and other drugs are Schedule II drugs, defined as “drugs with a high potential for abuse…with use potentially leading to severe psychological or physical dependence.”

Sound public policy must be based on facts, not radical unsafe, and dangerous theories.

This article is reproduced by the kind permission of The Daily Signal, the multimedia news site created by the Heritage Foundation in Washington DC.

New Hanover County is seeing an alarming trend of young children testing positive for drugs.

Child Protective Services handles a large number of substance abuse cases in parents, but discovering illegal substances in children was something they hardly expected. Kari Sanders, child protective services chief, said four children in the county, three years old and younger, recently tested positive for cocaine and marijuana. “In very severe cases, we have begun testing the children who are coming out of that environment, and it is very alarming that they are testing positive for drugs,” Sanders said.

Protective service officials used hair samples to test the children, but have no way of knowing how they came in contact with the drug. “It could possibly be second-hand. It could be due to the exposure in the home,” Sanders speculated. “It could be because they’re young children, toddlers, and they’re touching the substances in the home.”

While adults can receive treatment in drug rehabilitation facilities, young children have different needs and require specialized methods of treatment. “We’re being extremely diligent in ensuring that they’re getting regular pediatric care and their physician is aware that they tested positive, so they can take the appropriate action. Of course, we’re ensuring the children get developmental screenings so we can track their progress while they’re in our custody,” said Sanders about the process that happens after children are removed from their homes.

She said their main objective at Child Protective Services is to restore the children’s health and find a foster home for them, which is sometimes difficult. “I think there’s always a consistent need for foster parents, and we truly need foster parents who are in our community, in the same school districts that the children are coming from so children can remain in their home environment,” said Sanders about a statewide shortage of foster families.

“They may be removed from their home, but if we can keep other things consistent, like their school or daycare, that’s very important.”

Prenatal exposure to drugs can have long-term detrimental impact on the developing brain. Cocaine, for example, can readily cross the placenta and directly impact critical neurotransmitter systems in the foetal brain, including dopamine, serotonin, and norepinephrine systems. In a new study of the effects of prenatal cocaine exposure on brain structure, researchers found region-specific decreases in the volume of the cerebral cortex, thalamus, and putamen at 8-10 years of age in prenatally exposed children. Decreased volume of the thalamus and putamen, but not the cerebral cortex, was correlated with the reported level of maternal cocaine abuse. In addition, individuals who were prenatally exposed to cocaine had smaller average head circumference at birth through adolescence than unexposed children.

These findings highlight the vulnerability of the developing brain when exposed to cocaine in utero, leading to significant changes that are evident at least through adolescence.

RIO DE JANEIRO—Business was brisk in the Mandela shantytown on a recent night. In the glow of a weak light bulb, customers pawed through packets of powdered cocaine and marijuana priced at $5, $10, $25. Teenage boys with semiautomatic weapons took in money and made change while flirting with girls in belly-baring tops lounging nearby.

Next to them, a gaggle of kids jumped on a trampoline, oblivious to the guns and drug-running that are part of everyday life in this and hundreds of other slums, known as favelas, across this metropolitan area of 12 million people. Conspicuously absent from the scene was crack, the most addictive and destructive drug in the triad that fuels Rio’s lucrative narcotics trade.

Once crack was introduced here about six years ago, Mandela and the surrounding complex of shantytowns became Rio’s main outdoor drug market, a “cracolandia,” or crackland, where users bought the rocks, smoked and lingered until the next hit. Hordes of addicts lived in cardboard shacks and filthy blankets, scrambling for cash and a fix.

Now, there was no crack on the rough wooden table displaying the goods for sale, and the addicts were gone. The change hadn’t come from any police or public health campaign. Instead, the dealers themselves have stopped selling the drug in Mandela and nearby Jacarezinho in a move that traffickers and others say will spread citywide within the next two years.

The drug bosses, often born and raised in the very slums they now lord over, say crack destabilizes their communities, making it harder to control areas long abandoned by the government. Law enforcement and city authorities, however, take credit for the change, arguing that drug gangs are only trying to create a distraction and persuade police to call off an offensive to take back the slums. Dealers shake their heads, insisting it was their decision to stop selling crack, the crystalized form of cocaine.

“Crack has been nothing but a disgrace for Rio. It’s time to stop,” said the drug boss in charge. He is Mandela’s second-in-command—a stocky man wearing a Lacoste shirt, heavy gold jewelry and a backpack bulging with $100,000 in drugs and cash. At 37, he’s an elder in Rio’s most established faction, the Comando Vermelho, or Red Command. He’s wanted by police, and didn’t want his name published.

He discussed the decision as he watched the night’s profits pile up in neat, rubber-banded stacks from across the narrow street. He kept one hand on his pistol and the other on a crackling radio that squawked out sales elsewhere in the slum and warned of police. The talk of crack left him agitated; he raised his voice, drawing looks from the fidgety young men across the road. Although crack makes him a lot of money, he has his own reasons to resent the drug; everyone who comes near it does, he said.

His brother—the one who studied, left the shantytown and joined the air force—fell prey to it. Crack users smoke it and often display more addictive behavior. The brother abandoned his family and his job, and now haunts the edges of the slum with other addicts. “I see this misery,” he said. “I’m a human being too, and I’m a leader here. I want to say I helped stop this.”

For the ban to really take hold, it would need the support of the city’s two other reigning factions: the Amigos dos Amigos, or Friends of Friends, and the Terceiro Comando, Third Command. That would mean giving up millions in profits. According to an estimate by the country’s Security Committee of the House and the Federal Police, Brazilians consume between 800 kilos and 1.2 tons of crack a day, a total valued at about $10 million.

It’s unclear how much Rio’s traffickers earn from the drug, but police apprehensions show a surge in its availability in the state. In 2008, police seized 14 kilos; two years later the annual seizure came to 200 kilos, according to the Public Security Institute. Nonetheless, the other gangs are signing up, said attorney Flavia Froes. Her clients include the most notorious figures of Rio’s underbelly, and she has been shuttling between them, visiting favelas and far-flung high-security prisons to talk up the idea.

“They’re joining en masse. They realized that this experience with crack was not good, even though it was lucrative. The social costs were tremendous. This wasn’t a drug for the rich; it was hitting their own communities.”

As Froes walks these slums, gingerly navigating potholed roads in six-inch stiletto heels and rhinestone-studded jeans, men with a gun in each hand defer to her, calling her “doutora,” or doctor, because of her studies, or “senhora,” or ma’am, out of respect. “While stocks last, they’ll sell. But it’s not being bought anymore,” she said. “Today we can say with certainty that we’re looking at the end of crack in Rio de Janeiro.”

Even those who question the traffickers’ sudden surge of social conscience say the idea of the city’s drug lords coming together to ban crack isn’t far-fetched. After all, a similar deal between factions kept the drug out of Rio for years.

Crack first took hold in Sao Paulo, the country’s business capital, during the 1990s. In the early 2000s, it spread across Brazil in an epidemic reminiscent of the one the U.S. had experienced decades earlier. A recent survey found it was eventually sold or consumed in 98 percent of Brazilian municipalities. Most of the cities were too understaffed, underfunded and uninformed to resist its onslaught. And yet, an agreement between factions kept crack a rarity in Rio until a handful of years ago, said Mario Sergio Duarte, Rio state’s former police chief.

“Rio was always cocaine and marijuana,” he said. “If drug traffickers are coming up with this strategy of going back to cocaine and marijuana, it’s not because they suddenly developed an awareness, or because they want to be charitable and help the addicts. It’s just that crack brings them too much trouble to be worth it.”

Duarte believes dealers turned to crack when their other business started losing ground within the city.

Police started taking back slums long given over to the drug trade as Rio vied to host the 2014 World Cup and the 2016 Olympics. The plan disrupted trade, and the factions began hemorrhaging money, said Duarte. Crack seemed like the solution, and the drug flooded the market.

“Crack was profit; it’s cheap, but it sells. Addiction comes quick. They were trying to make up their losses,” he said. Soon, the gangs were being haunted by the consequences.

Unlike the customers who came for marijuana or cocaine, dropped cash and left, crack users hung around the sales points, scraping for money for the next hit. They broke the

social code that usually maintains a tense calm in the slums; they stole, begged, threatened or sold their bodies to get their next rock. Their presence made the hard life there nearly unbearable.

The Mandela drug boss said crack even sapped the drug kingpins’ authority. “How can I tell someone he can’t steal, when I know I sold him the drugs that made him this way?” he said. Many saw their own family members and childhood friends fall under the drug’s spell.

“The same crack I sell to your son is being sold to mine. I talked to one of the pioneers in selling crack in Rio. His son’s using now. Everyone is saying we have to stop.”

In Mandela, residents had to step over crack users on their way between home and work and warn their children to be careful around the “zombies.” “There were robberies in the favela, violence, people killed in the middle of the street, people having sex or taking a crap anywhere,” said Cleber, an electronics repair shop owner who has lived in Mandela for 16 years. He declined to give his last name because he lives in a neighborhood ruled by gang members, and like many, prefers not to comment publicly.

“Now we’re going out again, we can set up a barbecue pit outside, have a drink with friends, without them gathering around,” he said. “We’re a little more at ease.”

Researcher Ignacio Cano, at the Violence Analysis Center of Rio de Janeiro State University, said crack is still being sold outside only select communities and that it’s hard to tell if the stop is a temporary, local measure or a real shift in operations citywide. He said unprecedented pressure bore down on drug gangs once they began selling crack. In particular, the addicts’ encampments were sources of social and health problems, drawing the attention of the authorities.

Since March 2011, dawn raids involving police, health and welfare officials began taking users off the streets to offer treatment, food, a checkup and a hot shower. Since then, 4,706 people have cycled through the system. Of those, 663 were children or teenagers.

“I have operations every day, all over Rio,” said Daphne Braga, who coordinates the effort for the city welfare office. At the same time, crack became such a dramatic problem nationally that the government allocated special funds to combat it, including a $253 million campaign launched by President Dilma Rousseff in May 2010 to stem the drug trade. Last November, another $2 billion were set aside to create treatment centers for addicts and get them off the streets. In May, 150 federal police officers occupied a Rio favela to implement a pilot program fighting the crack trade and helping users.

“There are many reasons why they might stop,” said Cano.

Crack’s social cost is clear where the drug is still sold, right outside Mandela and Jacarezinho. In the shantytown of Manguinhos, along a violent area known as the Gaza Strip, an army of crack addicts lives in encampments next to a rail line.

Another couple hundred gather inside the slum, buying from a stand inside a little restaurant. Customers eat next to young men with guns and must step around a table laden with packaged drugs and tightly bound wads of cash to use the restroom. Crack users smoke outside, by the lights of a community soccer field where an animated game draws onlookers late into the night.

A 14-YEAR-old manages to get both the Prime Minister and Kevin Rudd’s wife Therese Rein on the phone, and the media flocks to his home in a bid to be the first to tell his side of the story.

This is not a child protege, nor is it a 14-year-old whose talents will deliver Olympic glory.

This Year 9 teenager is a convicted drug felon, having been caught buying 3.6g of marijuana on the streets of Kuta, and the fact that today he is at home is testament to the narrow escape he’s had from the claws of the Indonesian legal system.

His get-out-of-jail-free card is not a good luck charm he is likely to ever try again, but why after all the publicity generated by the cases of Schapelle Corby and the Bali Nine do so many continue to dice with death in Bali?

The answer is two-fold. Firstly, our acceptance of drugs inAustralia has now reached the point where we think it is relatively “normal” for a 14-year-old to have an addiction to a drug he has been smoking for two years.

A 2008 survey of 24,000 Australian high school students found that 14 per cent of students aged 12-to-17 years used cannabis, peaking at 26 per cent for 17-year-olds.

The Australian Secondary Students Alcohol and Drug survey found 80 per cent of pupils between 12 and 17 had tried alcohol. Eleven per cent of 12-year-olds had used inhalants in the previous month, and by the age of 17, seven per cent of students had used amphetamines.

So why would we raise our eyebrows when a 14-year-old Australian school student conducts a drug deal on the streets of Indonesia?

The catch here relates to where he bought the drugs and the penalties for drug-taking inAustralia, compared to our close neighbours – who make no secret of their bid to stamp it out.

Many, perhaps most, Australians are angry at Schapelle Corby’s on-going punishment, believing she has been unfairly treated. Thousands have signed petitions or offered prayers for those members of the Bali Nine who decided to wrap drugs to their bodies and smuggle it back home. Didn’t they think that other young Australians would use it – and possibly die?

Instead of ongoing outrage, we sympathise with those caught and point the finger of blame at Indonesia.

We have to change that psyche. Drugs are deadly. And in Indonesia the punishment for using them can be deadly too. It’s not a secret. And disagreeing with it doesn’t change it. In fact, in this part of the world,Australia is the odd one out, with other countries mirroring Indonesia’s stance.

So if we are serious about tackling drug use, we need to look at whether we should be ridiculing another country’s policy, or adopting tougher penalties here. Instead, we give movie-star status to a teenager who should know better. We protect him getting from the airport to his home, we don’t use his name, and his family breathes a sigh of relief that he’s relatively unscathed “considering what he went through”.

The next 14-year-old won’t receive the same easy ride, and this one is lucky authorities did not want to make an example of him – particularly at a time when we are laying down tough laws netting Indonesian teenagers lured into people-smuggling rackets in a bid to feed their families.

The problem with drugs is not Indonesia, or how it punishes users. The problem is with us, and how we have “normalised” drug use here – to the point where we’re told experimentation is typical in teenage years. To that extent, it’s not this lad’s fault either. The problem is bigger than he is, and will only grow while we accept its use and refuse to confront the consequences. The Courier-Mail spelt this out graphically in its Drug Scourge investigation, which showed greater crime, a bigger road toll and increasing mental health issues.

Several weeks ago on the Gold Coast, I walked into the female toilets used by diners of an upmarket restaurant to see a well-dressed young man sniffing cocaine off a toilet seat. He apologised – for using the female toilet not the drug-taking – and continued on his high. No shame, but is there any wonder?

Your article about drugs is not backed up by the evidence, there is plenty of scope for drugs use to increase under a change of system where drugs use is normalised (either decrimininalisation or various legalization models). The evidence is in the tobacco/alcohol model /as variously applied/ around the world. Tobacco and alcohol cause far more /total harm/ than the illegal drugs simply through prevalence.

Your remarks about Portugal are not supported by a critical examination of what has taken place there. All the hyperbole about Portugal as a model is based on one flawed study, assiduously reported around the world as a “meme” by the George Soros financed, world-wide, legalisation campaign. You have been hoodwinked. Not surprising really, millions of dollars have been spent to do that to you.

Portugal and decriminalisation appears now to be “the new orthodoxy” for those with a certain direction of travel and for those “user advocates” who want more freedom to use, regardless of the wider social effects.

Portugal is being misrepresented

1. The number of new cases of HIV and Hepatitis C inPortugalis eight times the average in other EU countries

2.Portugal has the most cases of injected drug related AIDS with 85 new cases per one million citizens. Other EU countries averaging 5 per million.

Finally the suggestion made by some, that legalisation would somehow remove criminality from drug supply is ridiculous. Criminality loves use-reinforcing substances and behaviours. More than 20% of the UK tobacco market is smuggled, counterfeit, or both. In some other countries it is much worse.

Legalisation or decriminalisation, of substances unfit for human consumption, should only occur if a demonstrable “public good” can be evidenced.

Illegal drugs not only harm a user’s mind and body, they devastate families, communities, and neighborhoods. They jeopardize public safety, prevent too many Americans from reaching their full potential, and place obstacles in the way of raising a healthy generation of young people.

To address these challenges, today we are releasing the 2012 National Drug Control Strategy — the Obama Administration’s primary policy blueprint for reducing drug use and its consequences in America. The President’s inaugural National Drug Control Strategy, published in 2010, charted a new direction in our approach to drug policy. Today’s strategy builds upon that approach, which is based on science, evidence, and research. Most important, it is based on the premise that drug addiction is a chronic disease of the brain that can be prevented and treated. Simply put, we are not powerless against the challenge of substance abuse — people can recover, and millions are in recovery. These individuals are our neighbors, friends and family members. They contribute to our communities, our workforce, our economy, and help make America stronger.

Our emphasis on addressing the drug problem through a public health approach is grounded in decades of research and scientific study. There is overwhelming evidence that drug prevention and treatment programs achieve meaningful results with significant long-term cost savings. In fact, recent research has shown that each dollar invested in an evidence-based prevention program can reduce costs related to substance use disorders by an average of $18.

But reducing the burden of our nation’s drug problem stretches beyond prevention and treatment. We need an all of the above approach. To address this problem in a comprehensive way, the President’s new strategy also applies the principles of public health to reforming the criminal justice system, which continues to play a vital role in drug policy. It outlines ways to break the cycle of drug use, crime, incarceration, and arrest by diverting non-violent drug offenders into treatment, bolstering support for reentry programs that help offenders rejoin their communities, and advancing support for innovative enforcement programs proven to improve public health while protecting public safety.

Together, we have achieved significant reform in the way we address substance abuse. And the Affordable Care Act will — for the first time — require insurers to cover treatment for drug addiction the same way they would other chronic diseases. This is a revolutionary shift in how we address drug policy in America.
Over the past three decades, we have reduced illegal drug use in America. Over the long term, rates of drug use among young people today are far lower than they were 30 years ago. More recently cocaine use has dropped nearly 40 percent and meth use has dropped by half. And we can do more. As President Obama has noted, we have successfully changed attitudes regarding rates of smoking and drunk driving, and with your help we can do the same with our illegal drug problem.

Source: R. Gil Kerlikowske
Director, White House Office of National Drug Control Policy 18th April 2012

149,100 In 2010, coca was cultivated on 149,100 hectares in the Andean countries – an area roughly one and a half times the size of Hong Kong – down from 221,300 hectares in 2000.

6% In 2010, the global area under coca cultivation decreased by 6%, mainly due to a significant reduction in Colombia that was not entirely offset by a small increase in Peru.

732,000 The amount of cocaine seized worldwide in 2009 was 732,000kg – which refers to seizures unadjusted for purity. The United Nations Office on Drugs and Crime estimates that between 46% and 60% of cocaine produced was seized – an indication of the amount manufactured the previous year.

444,000 The best reading of data and estimates suggests that about 440,000kg of pure cocaine was consumed worldwide in 2009. This would be in line with a production estimate of about 1.1m kg and purity adjusted seizures of 615,000kg, plus agricultural and other losses of about 55,000kg (which represents 5% of production).

$85bn The value of the global cocaine market is lower than in the mid-1990s, when prices were much higher and the US market was strong. In 1995, the global market was worth about $165bn, while, in 2009, this had been reduced to just over half of that.

99% Of that $85bn income from global cocaine retail sales in 2009, traffickers are estimated to have reaped about $84bn (almost 99%). The rest went to Andean farmers.

5m The US has the highest prevalence of cocaine use (2.4% of the population, or five million people, aged 15-64), but there are indications of cocaine use declining in the last few years.

$33bn The amount of cocaine consumed in Europe has doubled in the last decade. The volume and value of the western and central European cocaine market, currently valued at $33bn, is now approaching parity with that of the US ($37bn).

80% Two thirds of European cocaine users live in three countries: the UK, Spain and Italy. With Germany and France, these countries represent 80% of European cocaine consumption.

272m Globally, the UN Office on Drugs and Crime estimates that between 149 and 272 million people – 3.3%-6.1% of the population aged 15-64 – used illicit drugs at least once in the previous year.

Nicotine appears to be a “gateway” drug that primes the brain to be susceptible to cocaine, according to a new study in mice. The researchers say if further studies show the findings apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction, the Los Angeles Times reports.

The study found mice exposed to nicotine in drinking water for at least seven days showed an increased response to cocaine. The researchers also looked at data on cocaine use among a group of high school students, and found 81 percent of those who started using cocaine did so in a month when they were smoking tobacco.

The findings appear in the journal Science Translational Medicine. Previous studies have shown that most illegal drug users report using tobacco products or alcohol before they started illicit drug use, according to a news release by the National Institute on Drug Abuse, which funded the study. Until now, studies have not shown a biological mechanism through which exposure to nicotine increases vulnerability to illegal drug use, the release notes.

“Now that we have a mouse model of the actions of nicotine as a gateway drug this will allow us to explore the molecular mechanisms by which alcohol and marijuana might act as gateway drugs,” lead author Eric Kandel, MD, of Columbia University Medical Center, said in the release. “In particular, we would be interested in knowing if there is a single, common mechanism for all gateway drugs or if each drug utilizes a distinct mechanism.”

Guernsey’s Health and Social Services Department has issued a warning about the danger of a toxic chemical found locally in cocaine. The department said levamisole had been detected in recent samples of the drug. It said that some people who ingested the chemical developed agranulocytosis, a potentially fatal condition that harms the immune system. Dr Roland Archer, the States analyst, said: “This is the first time that it has been detected in Guernsey.” He said: “Once levamisole has been added to cocaine, it is nearly impossible to remove it and it even survives processing of cocaine into ‘crack’.” New equipment costing £80,000 has enabled the department to examine drugs at a molecular level. A gas chromatograph mass spectrometer, recently purchased by the department, helped find the substance. Dr Archer said: “It gives us a lot more confidence when presenting the data on controlled drugs.”

A single 15-minute exposure to nicotine caused a long-term increase in the excitability of neurons involved in reward, according to a study published in The Journal of Neuroscience. The results suggest that nicotine and cocaine hijack similar mechanisms of memory on first contact to create long-lasting changes in a person’s brain.
“Of course, for smoking it’s a very long-term behavioral change, but everything starts from the first exposure,” said Danyan Mao, PhD, postdoctoral researcher at the University of Chicago Medical Center. “That’s what we’re trying to tackle here: when a person first is exposed to a cigarette, what happens in the brain that might lead to a second cigarette?”
Learning and memory are thought to be encoded in the brain via synaptic plasticity, the long-term strengthening and weakening of connections between neurons. When two neurons are repeatedly activated together, a stronger bond forms between them, increasing the ability of one to excite the other.
Previous research in the laboratory of Daniel McGehee, PhD, neuroscientist and associate professor in the Department of Anesthesia & Critical Care at the Medical Center, discovered that nicotine could promote plasticity in a region of the brain called the ventral tegmental area (VTA). Neurons that originate in the VTA release the neurotransmitter dopamine, known to play a central role in the effects of addictive drugs and natural rewards such as food and sex.
“We know that a single exposure to physiologically relevant concentrations of nicotine can lead to changes in the synaptic drive in the circuitry that lasts for several days,” said McGehee, senior author of this study. “That idea is very important in how addiction forms in humans and animals.”
In the new experiments, Mao monitored the electrical activity of VTA dopamine neurons in slices of brain dissected from adult rats. Each slice was bathed for 15 minutes in a concentration of nicotine similar to the amount that would reach the brain after smoking a single cigarette. After 3-5 hours, Mao conducted electrophysiology experiments to detect the presence of synaptic plasticity and determine which neurotransmitter receptors were involved in its development.
Mao discovered that nicotine-induced synaptic plasticity in the VTA is dependent upon one of the drug’s usual targets, a receptor for the neurotransmitter acetylcholine located on the dopamine neurons. But another element found necessary for nicotine’s synaptic effects was a surprise: the D5 dopamine receptor, a component previously implicated in the action of cocaine. Blocking either of these receptors during nicotine exposure eliminated the drug’s ability to cause persistent changes in excitability.
“We found that nicotine and cocaine employ similar mechanisms to induce synaptic plasticity in dopamine neurons in VTA,” Mao said.
While the subjective effects of nicotine and cocaine are very different in humans, the overlapping effects of the two drugs on the reward system of the brain may explain why both are highly addictive substances, the researchers said.
“We know without question that there are big differences in the way these drugs affect people,” McGehee said. “But the idea that nicotine is working on the same circuitry as cocaine does point to why so many people have a hard time quitting tobacco, and why so many who experiment with the drug end up becoming addicted.”
The overlap between nicotine and cocaine effects at the D5 receptor may also offer a novel strategy for preventing or treating addiction. However, currently-known blockers of the receptor also block another dopamine receptor, D1, that is important for normal, healthy motivation and movement.
“This dopamine receptor is attractive as a potential target,” McGehee said. “The real challenge is to tweak the addictive effect of drugs like nicotine or other psychostimulants without totally crushing the person’s desire to pursue healthy behavior.”
Future research will also focus on whether repeated exposure to nicotine, as would occur in a regular smoker, changes the drug’s effects on synaptic plasticity in the VTA. In the meantime, the current study builds evidence that addictive drugs appropriate the neurobiological tools of learning and memory to create long-term changes in brain reward pathways.
“It’s all fitting with the overriding idea that changes in synaptic strength are part of the way these drugs motivate behavior in a persistent way,” McGehee said.
The study, “Nicotine Potentiation of Excitatory Inputs to Ventral Tegmental Dopamine Neurons,” will be published May 4, 2011 by The Journal of Neuroscience. In addition to Mao and McGehee, Keith Gallagher of the University of Chicago is a co-author.
The research was supported by grants from the Women’s Council of the Brain Research Foundation and the National Institutes of Health.

Source: University of Chicago Medical Center (2011, May 4). Nicotine and cocaine leave similar mark on brain after first contact. ScienceDaily. Retrieved May 8, 2011, from http://www.sciencedaily.com¬ /releases/2011/05/110503171745.htm

Prescription narcotics were involved in more drug overdose deaths in 2007 than heroin and cocaine combined, according to a new article. And in some states, the number of deaths from prescription painkiller overdose is higher than suicide or car crashes.
Approximately 27,500 people died from unintentional prescription narcotics overdoses in 2007, driven to a large extent by prescription narcotics overdoses, said researchers from the Centers for Disease Control and Prevention (CDC), Duke University and the University of North Carolina at Chapel Hill. Narcotics pain medications were also involved in about 36 percent of all poisoning suicides in the U.S. in 2007.
many deaths from both Operation Iraqi Freedom and Operation Enduring Freedom in Afghanistan, from the beginning of both wars through Feb. 20, 2011, said study researcher Dr. Richard H. Weisler, an adjunct professor of psychiatry at UNC Chapel Hill and Duke University.
Alternatively, the drug overdose deaths would be equivalent to losing an airplane carrying 150 passengers and crew every day for six months, researchers said.
The study findings come on the tail of another article published this month in the Journal of the American Medical Association, which showed that the risk of fatal overdose increases with the dose of drugs taken (though taking the medications as needed or as prescribed was not associated with overdose risk).
In 2009, the CDC’s National Youth Risk Behavior Survey revealed that 1 in 5 high school students in the United States have abused prescription drugs, including the narcotics painkillers OxyContin, Percocet and Vicodin. Narcotics, also called opioids, are synthetic versions of opium that are used to treat moderate and severe pain.
And in June last year, the CDC reported that visits to hospital emergency departments involving nonmedical use of prescription narcotic pain relievers has more than doubled, rising 111 percent, between 2004 and 2008.
Researchers said one of the key reasons for the increase in prescription drug overdose deaths is increased nonmedical use of narcotics without a prescription because of the feeling it produces. They also said that medical providers, psychiatrists and primary care physicians may fail to anticipate the extent of overlap between chronic pain, mental illness and substance abuse among their patients.
For example, 15 percent to 30 percent of people with unipolar, bipolar, anxiety, psychotic, non-psychotic and attention deficit/hyperactivity disorders will also have substance abuse problems, said study researcher Dr. Ashwin A. Patkar, associate professor of psychiatry and behavioral sciences at Duke University.
“Similarly, people with substance abuse are more likely to have another mental illness and a significant number of patients with chronic pain will have mental illness or substance abuse problems,” Patkar said in a statement.
Moreover, narcotics, benzodiazepines, antidepressants and sleep aids are commonly prescribed even though they are harmful and addictive when abused, researchers said. It’s the combinations of these drugs that are frequently found in the toxicology reports of people dying of overdoses.
Researchers suggest that before prescribing narcotics, doctors should try non-narcotic medications as well as — when possible — physical therapy, psychotherapy, exercise and other nonmedicinal methods.
The study was published last week in the Journal of Clinical Psychiatry.
Pass it on: Overdosing on narcotic painkillers accounts for more deaths than from heroin and cocaine combined.

Brain abnormalities could be help explain why certain people could have a pre-disposition to cocaine dependency, according to research published today.

In a report in The Herald newspaper today, researchers at theUniversity of Cambridge have identified the abnormalities in the frontal lobe of cocaine users’ brains which are linked to their compulsive cocaine-using behaviour. Scientists think these abnormalities could help explain why some people are more prone to drug dependency.

The researchers, led by Dr Karen Ersche of the University’s Behavioural and Clinical Neuroscience Institute, scanned the brains of 120 people, half of whom had a dependence on cocaine. They found that the cocaine users had widespread loss of grey matter which was directly related to the duration of their cocaine use and that this reduction in volume was associated with greater compulsivity to take cocaine.

The scientists also found that parts of the brain reward system where cocaine exerts its actions were significantly enlarged in cocaine users. This was not linked to the duration of the user’s habit.

The researchers believe this may suggest that alterations in the brain’s reward system predate cocaine use, possibly making these individuals more vulnerable to the effects of the drug.

The Advisory Council on the Misuse of Drugs is currently carrying out a review of the harms associated with cocaine.

Abstract

OBJECTIVE:

Prenatal cocaine exposure has been associated with alterations in neonatal behavior and more recently a dose-response relationship has been identified. However, few data are available to address the long-term behavioral effects of prenatal exposures in humans. The specific aim of this report is to evaluate the school-age behavior of children prenatally exposed to cocaine.

METHODS:

All black non-human immunodeficiency virus-positive participants in a larger pregnancy outcomes study who delivered singleton live born infants between September 1, 1989 and August 31, 1991 were eligible for study participation. Staff members of the larger study extensively screened study participants during pregnancy for cocaine, alcohol, cigarettes, and other illicit drugs. Prenatal drug exposure was defined by maternal history elicited by structured interviews with maternal and infant drug testing as clinically indicated. Cocaine exposure was considered positive if either history or laboratory results were positive. Six years later, 665 families were contacted; 94% agreed to participate. The child, primary caretaker (parent), and, when available, the biologic mothers were tested in our research facilities. Permission was elicited to obtain blinded teacher assessments of child behavior with the Achenbach Teacher’s Report Form (TRF). Drug use since the child’s birth was assessed by trained researchers using a structured interview.

RESULTS:

Complete laboratory and teacher data were available for 499 parent-child dyads, with a final sample size for all analyses of 471 (201 cocaine-exposed) after the elimination of mentally retarded subjects. A comparison of relative Externalizing (Aggressive, Delinquent) to Internalizing (Anxious/Depressed, Withdrawn, Somatic Complaints) behaviors of the offspring was computed for the TRF by taking the difference between the 2 subscales to create an Externalizing-Internalizing Difference (T. M. Achenbach, personal communication, 1998). Univariate comparisons revealed that boys were significantly more likely to score in the clinically significant range on total TRF, Externalizing-Internalizing, and Aggressive Behaviors than were girls. Children prenatally exposed to cocaine had higher Externalizing-Internalizing Differences compared with controls but did not have significantly higher scores on any of the other TRF variables. Additionally, boys prenatally exposed to cocaine were twice as likely as controls to have clinically significant scores for externalizing (25% vs 13%) and delinquent behavior (22% vs 11%). Gender, prenatal exposures (cocaine and alcohol), and postnatal risk factors (custody changes, current drug use in the home, child’s report of violence exposure) were all related to problem behaviors. Even after controlling for gender, other prenatal substance exposures, and home environment variables, cocaine-exposed children had higher Externalizing-Internalizing Difference scores. Prenatal exposure to alcohol was associated with higher total score, increased attention problems, and more delinquent behaviors. Prenatal exposure to cigarettes was not significantly related to the total TRF score or any of the TRF subscales. Postnatal factors associated with problem behaviors included both changes in custody status and current drug use in the home. Change in custody status of the cocaine-exposed children, but not of the controls, was related to higher total scores on the TRF and more externalizing and aggressive behaviors. Current drug use in the home was associated with higher scores on the externalizing and aggressive subscales.

CONCLUSIONS:

Results of this study suggest gender-specific behavioral effects related to prenatal cocaine exposure. Prenatal alcohol exposure also had a significant impact on the TRF. Postnatal exposures, including current drug use in the home and the child’s report of violence exposure, had an independent effect on teacher-assessed child behavioral problems.

The blood pressure drug propranolol may help treat cocaine addiction, a new animal study suggests. The study investigated the behavior of rats repeatedly given injections of cocaine in a particular cage. The rats learned to associate the positive feelings of cocaine with the cage, much as humans associate the high of cocaine with the environment in which they use the drug, Time reports.

The researchers found that rats given propranolol before they were allowed to enter the cocaine cage, no longer showed a preference for it over any other cage. Rats who were given shots of saline instead of the blood pressure drug continued to seek out the cocaine cage for at least two weeks.

In humans, propranolol might dull the pleasant associations of cocaine, the article says. The cravings that accompany those feelings might also dissipate, and that in turn could reduce the risk of a relapse. The article notes that propranolol has been studied as a treatment for post-traumatic stress disorder, with mixed results.

Abstract

A review of the existing literature on the occurrence of challenging behavior among children with prenatal drug exposure was conducted. While a large number of studies were identified that evaluated various outcomes of prenatal drug exposure, only 37 were found that directly evaluated challenging behaviors. Of the 37 studies, 23 focused on prenatal cocaine exposure, and 14 focused on prenatal alcohol exposure; most studies relied on broadband measures such as the CBCL for the assessment of challenging behavior. Among the 37 studies, a clear role for the postnatal environment on developing challenging behaviors was evident; however, prenatal alcohol exposure showed a much clearer independent effect upon challenging behaviors than was noted in the prenatal cocaine studies. Additionally, only 3 of the 37 studies addressed interventions for challenging behaviors, each of which showed an improvement in child behavior or parent-child interactions. As researchers have continued to show the importance of the postnatal environment, it is likely that interventions addressing specific environmental risk factors will be helpful to reduce or prevent challenging behaviors among this population.

People addicted to cocaine have an impaired ability to perceive rewards and exercise control due to disruptions in the brain’s reward and control circuits, according to a series of brain-mapping studies and neuropsychological tests conducted at the U.S. Department of Energy’s Brookhaven National Laboratory.
“Our findings provide the first evidence that the brain’s threshold for responding to monetary rewards is modified in drug-addicted people, and is directly linked to changes in the responsiveness of the prefrontal cortex, a part of the brain essential for monitoring and controlling behavior,” said Rita Goldstein, a psychologist at Brookhaven Lab. “These results also attest to the benefit of using sophisticated brain-imaging tools combined with sensitive behavioral, cognitive, and emotional probes to optimize the study of drug addiction, a psychopathology that these tools have helped to identify as a disorder of the brain.”
Goldstein will present details of these studies at a press conference on neuroscience and addiction at the Society for Neuroscience (SfN) annual meeting in Atlanta, Georgia, on Sunday, October 15, 2006, 2 to 3 p.m., and at a SfN symposium on Wednesday, October 18, 8:30 a.m.
Goldstein’s experiments were designed to test a theoretical model, called the Impaired Response Inhibition and Salience Attribution (I-RISA) model, which postulates that drug-addicted individuals disproportionately attribute salience, or value, to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli – with a concomitant decrease in the ability to inhibit maladaptive drug use. In the experiments, the scientists subjected cocaine-addicted and non-drug-addicted individuals to a range of tests of behavior, cognition/thought, and emotion, while simultaneously monitoring their brain activity using functional magnetic resonance imaging (fMRI) and/or recordings of event-related potentials (ERP).
In one study, subjects were given a monetary reward for their performance on an attention task. Subjects were given one of three amounts (no money, one cent, or 45 cents) for each correct response, up to a total reward of $50 for their performance. The researchers also asked the subjects how much they valued different amounts of monetary reward, ranging from $10 to $1000.
More than half of the cocaine abusers rated $10 as equally valuable as $1000, “demonstrating a reduced subjective sensitivity to relative monetary reward,” Goldstein said.
“Such a ‘flattened’ sensitivity to gradients in reward may play a role in the inability of drug-addicted individuals to use internal cues and feedback from the environment to inhibit inappropriate behavior, and may also predispose these individuals to disadvantageous decisions – for example, trading a car for a couple of cocaine hits. Without a relative context, drug use and its intense effects – craving, anticipation, and high – could become all the more overpowering,” she said.
The behavioral data collected during fMRI further suggested that, in the cocaine abusers, there was a “disconnect” between subjective measures of motivation (how much they said they were engaged in the task) and the objective measures of motivation (how fast and accurately they performed on the task).
“These behavioral data implicate a disruption in the ability to perceive inner motivational drives in cocaine addiction,” Goldstein said.
The fMRI results also revealed that non-addicted subjects responded to the different monetary amounts in a graded fashion: the higher the potential reward, the greater the response in the prefrontal cortex. In cocaine-addicted subjects, however, this region did not demonstrate a graded pattern of response to the monetary reward offered. Furthermore, within the cocaine-addicted group, the higher the sensitivity to money in the prefrontal cortex, the higher was the motivation and the self-reported ability to control behavior.
The ERP results showed a similarly graded brain response to monetary reward in healthy control subjects, but not in cocaine-addicted individuals.
“The dysfunctional interplay between reward processing and control of behavior observed in these studies could help to explain the chronically relapsing nature of drug addiction,” Goldstein said. “Our results also suggest the need for new clinical interventions aimed at helping drug abusers manage these symptoms as part of an effective treatment strategy.”

Mount Sinai researchers have discovered how cocaine corrupts the brain and becomes addictive. These findings — the first to connect activation of specific neurons to alterations in cocaine reward — were published in Science on October 15. The results may help researchers in developing new ways of treating those addicted to the drug.

Led by Mary Kay Lobo, PhD, Postdoctoral Fellow in the Department of Neuroscience at Mount Sinai School of Medicine and first author of the study, researchers found that the two main neurons (D1 and D2) in the nucleus accumbens region of the brain, an important part of the brain’s reward center, exert opposite effects on cocaine reward. Activation of D1 neurons increases cocaine reward whereas activation of D2 neurons decreases cocaine reward.
“The data suggest a model whereby chronic exposure to cocaine results in an imbalance in activity in the two nucleus accumbens neurons: increased activity in D1 neurons combined with decreased activity in D2 neurons,” said Dr. Lobo. “This further suggests that BDNF-TrkB signaling in D2 neurons mediates this decreased activity in D2 neurons.”
The study was conducted using optogenetics, a technology to optically control neuronal activity in freely moving rodents.

Opposite cocaine reward similar to those found when activating each neuron is achieved by disrupting brain-derived neurotrophic factor, which is a protein in the brain known for its involvement in neuronal survival, learning, and memory and drug abuse signaling through its receptor TrkB in D1 or D2 neurons.

“This new information provides fundamentally novel insight into how cocaine corrupts the brains reward center, and in particular how cocaine can differentially effect two neuronal subtypes that are heterogeneously intermixed in the nucleus accumbens,” said Eric Nestler, MD, PhD, Chair of Neuroscience, Nash Family Professor, and Director of The Friedman Brain Institute at Mount Sinai and co-author on the study. “We can use this information to potentially develop new therapies for cocaine addiction, possibly aimed at altering neuronal activity selectively in either neuronal subtype.”

Cocaine is one of the oldest drugs known to humans, and its abuse has become widespread since the end of the 19th century. At the same time, we know rather little about its effects on the human brain or the mechanisms that lead to cocaine addiction. The latest article by Dr. Marco Leyton, of the Montreal Neurological Institute (MNI), McGill University and the McGill University Health Centre, which was published in the journal Biological Psychiatry on May 15, 2009, not only demonstrates a link between cocaine and the reward circuits in the brain but also associates the susceptibility to addiction with these mechanisms.

The results of this study show that sniffing cocaine triggers high levels of dopamine secretion in a central region of the brain called the striatum. Dopamine is known to play a critical role in the brain’s response to reward as well as in its response to addictive drugs.
This study was carried out in ten non-addicted users of cocaine, all of whom sniffed cocaine on one test day and placebo powder on another. Participants underwent blood tests before and after taking the drug, and dopamine release in the brain was measured using PET scans.
“The ability of cocaine to activate dopamine release varies markedly from person to person. Our study suggests that this is related to how much of the drug the person consumed in the past,” explained Dr. Leyton. The more cocaine someone has used in his or her lifetime, the more the brain will secrete dopamine during subsequent cocaine use. “It’s possible therefore that the intensity of the reward-circuit response is related to increased susceptibility to addiction,” stated Dr. Leyton.
Although the relationship between the intensity of dopamine secretion and the frequency of drug use has been demonstrated, researchers still do not fully understand its mechanism of action. Is it the repeated stimulation of the reward circuit that leads to addiction, or is it an inherent sensitivity to addiction that leads to the increased secretion of dopamine? This question is not easy to answer, especially since other factors come into play, such as other aspects of the subject’s personal history.
Whatever the answer, the relationship between dopamine and cocaine means that this hormone could be a potential target for treatment against addiction. More research is required before treatments are available, but this study opens a new door in this direction.
This study was funded with a grant from the Canadian Institutes for Health Research. Salary support was given by the Fond de recherche en santé du Québec
This study is a collaboration between several laboratories of the McGill University Health Centre and McGill University, involving : Dr Sylvia M.L. Cox, Dr Chawki Benkelfat, Dr Alain Dagher, Dr J. Scott Delaney, France Durand, Samuel A. McKenzie, Dr Theodore Kolivakis, Kevin F. Casey, Dr Marco Leyton.

Environmental conditions play a major role in treating drug addiction and in preventing relapses, according to new research. For the first time, researchers from the Institut de physiologie et biologie cellulaire (CNRS/Université de Poitiers) have shown that positive and stimulating environmental conditions make it easier to treat cocaine addiction.

Even though numerous data exist on the mechanisms of cocaine addiction, there are as yet no effective therapies, making it very urgent that new strategies for treating the disease be developed. According to a study by Marcello Solinas and Mohamed Jaber, carried out by a group of researchers at the Institut de physiologie et biologie cellulaire in Poitiers, exposing mice to an “enriched environment (1)” during cocaine withdrawal removes abnormal behavior related to addiction. An enriched environment, for mice, is an environment which stimulates their curiosity, providing social and physical activity as well as exploration.
After addicting animals to cocaine, the researchers then exposed them to an enriched environment made up of large cages with a small house, a running wheel, tunnels and other appealing toys which were changed weekly.
Three models of animal addiction were used:
behavioral sensitization, which measures the progressive increase in the stimulating effects of cocaine after chronic administration;
the location preference, which measures the ability of a context (associated with cocaine consumption) to lead to drug-seeking behavior, and the renewal of this drug-induced location preference;
measurements of cocaine’s ability to lead to a relapse after a period of withdrawal.
The result was that after thirty days of exposure to an enriched environment, addiction behavior typical of these three models had disappeared.
To identify the brain areas involved in the beneficial effect of an enriched environment, the researchers used an approach from functional neuro-anatomy. They showed that the absence of relapse in “enriched” mice was associated with a decrease in the cocaine-induced activation of a set of brain structures involved in dopaminergic transmission and associated with relapse.
These results, which have both a medical and societal impact, suggest that the living conditions of drug addicts should be taken into account in determining their therapy. A real effort should be made to create enriched environmental conditions, providing patients with different types of social, physical and intellectual stimulation. This also suggests that under deprived environmental conditions, treating addiction can be very challenging.
Note:
1) A number of earlier studies had shown that when animals are raised in an enriched environment prior to drug exposure, their vulnerability to addiction was reduced. In such conditions, the enriched environment can be seen as preventive.

Addictive drugs are known to induce changes in the brain’s reward circuits that may underlie drug craving and relapse after long periods of abstinence. Now, new research in the September 9 issue of the journal Neuron, uncovers a specific neural mechanism that may be linked to persistent drug-seeking behavior and could help to guide strategies for development of new therapies for cocaine addiction.

Previous research has shown that the ventral tegmental area (VTA) is a brain region that is activated when cocaine users experience a craving for cocaine after being exposed to cocaine-associated cues. The medial prefrontal cortex (mPFC), which receives input from the VTA via circuits that use the “reward” neurotransmitter dopamine, has also been implicated in drug craving after cocaine withdrawal. Further, increases in the level of brain-derived neurotrophic factor (BDNF) have been observed in the VTA and mPFC in rats after withdrawal from repeated cocaine exposure.
“BDNF plays a key role in modulating the structure and function of synapses, the sites of communication between neurons. Therefore, increased BDNF after cocaine withdrawal may drive synaptic changes that contribute to compulsive drug seeking behavior,” explains senior author, Dr. Mu-ming Poo from the University of California, Berkeley. “It has been shown that increased BDNF in the VTA after cocaine withdrawal in rats promotes the drug-dependent motivational state. However, nothing is known about the potential BDNF effect on synaptic function and plasticity in mPFC neurons after cocaine withdrawal.”
Dr. Poo and colleagues designed a study to examine how BDNF and the mPFC might contribute to relapse after cocaine addiction. The researchers found that the gradual increase in BDNF expression in the rat mPFC after terminating repeated cocaine exposure significantly enhanced the activity-induced potentiation of specific synapses. Dr. Poo’s group went on to uncover the specific cellular mechanism linking increased BDNF with enhanced synaptic plasticity and demonstrated that interference with the key molecule in the BDNF signaling process reduced behavioral sensitivity after cocaine withdrawal in rats.
“In short, our results demonstrate that elevated BDNF expression after cocaine withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity-induced persistent potentiation that may contribute to cue-induced drug cravings and drug-seeking behavior,” concludes Dr. Poo. Although a clear correlation between rat and human behaviors of cocaine craving and relapse remains to be established, the cellular mechanism uncovered in this study does appear to have behavioral relevance and may represent a direct brain sensitization that is involved in triggering relapse.
The researchers include Hui Lu, Pei-lin Cheng, Byung Kook Lim, Nina Khoshnevisrad, and Mu-ming Poo, University of California, Berkeley, Berkeley, CA.

Doctors have used the drug disulfiram to help patients stay sober for several decades. It interferes with the body’s ability to metabolize alcohol, giving a fierce hangover to someone who consumes even a small amount of alcohol.
More recently, disulfiram was shown to be effective in treating cocaine addiction as well, even though alcohol and cocaine affect the nervous system in different ways.
Now, researchers at Emory University School of Medicine have identified how disulfiram may exert its effects, and have shown that a newer drug with fewer side effects works by the same mechanism.
The results are published online this week by the journal Neuropsychopharmacology. Research assistant professor Jason Schroeder, PhD, and graduate student Debra Cooper are co-first authors of the paper, and the research also involved collaborations with P. Michael Iuvone, PhD, director of research at the Emory Eye Center, Gaylen Edwards, DVM, PhD, head of the department of physiology and pharmacology at the University of Georgia’s College of Veterinary Medicine, and Philip Holmes, PhD, professor of psychology at the University of Georgia.
“Disulfiram has several effects on the body: it interferes with alcohol metabolism, but it inhibits several other enzymes by sequestering copper, and can also damage the liver,” says senior author David Weinshenker, PhD, associate professor of human genetics at Emory University School of Medicine. “We wanted to figure out how disulfiram was working so we could come up with safer and potentially more effective treatments.”
In treating cocaine addiction, there are several challenges: not only getting people to stop taking the drug, but also preventing relapse. Cocaine boosts the levels of several neurotransmitters, including dopamine and norepinephrine, at the junctions between nerve cells by blocking the machinery the brain uses to remove them.
Under normal conditions, dopamine is important for the sensation of pleasure produced by natural rewards such as food or sex, Weinshenker says. Cocaine “hijacks” the dopamine system, which plays a large role in addiction. Similarly, norepinephrine has a role in attention and arousal, but its overactivation can trigger stress responses and relapse, he says.
Weinshenker’s team showed that disulfiram prevents rats from seeking cocaine after a break, a model for addicts tempted to relapse. At the same time, it doesn’t stop them from taking cocaine when first exposed to it, or from enjoying their food.
Disulfiram appears to work by inhibiting dopamine beta-hydroxylase, an enzyme required for the production of norepinephrine. A dose of disulfiram that lowers the levels of norepinephrine in the brain by about 40 percent is effective, while doses that do not reduce norepinephrine have no effect on relapse-like behavior in rats.
To confirm that the beneficial effects of disulfiram were because of dopamine beta-hydroxylase inhibition, the researchers turned to a drug called nepicastat, which was originally developed for the treatment of congestive heart failure in the 1990s.
“Nepicastat is a selective dopamine beta-hydroxylase inhibitor that does not sequester copper or impair a host of other enzymes like disulfiram,” Weinshenker says. “We reasoned that if disulfiram is really working through dopamine beta-hydroxylase, then nepicastat might be a better alternative.”
Researchers at the University of Texas Medical Branch at Galveston have recently completed a Phase I safety trial studying nepicastat for the treatment of cocaine addiction in human subjects.
Weinshenker is co-inventor on a patent on the use of dopamine beta-hydroxylase inhibitors for the treatment of cocaine dependence, and could benefit from their commercialization. This has been reviewed by Emory University’s Conflict of Interest Committee, and a management plan is in place.
The research was supported by the National Institute of Drug Abuse and the National Eye Center.

A typical drug user’s transition to addiction could result from a persistent impairment of synaptic plasticity in a key structure of the brain, suggests a new French study.
The research, by the teams of Pier Vincenzo Piazza and Olivier Manzoni, at the Neurocentre Magendie in Bordeaux, appears in the journal Science.

This study is the first demonstration that a correlation exists between synaptic plasticity and the transition to addiction. The results from the teams at Neurocentre Magendie call into question the hitherto held idea that addiction results from pathological cerebral modifications, which develop gradually with drug usage.

Their results show that addiction may, instead, come from a form of anaplasticity, i.e. from incapacity of addicted individuals to counteract the pathological modifications caused by the drug to all users.

The voluntary consumption of drugs is a behaviour found in many species of animals. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is behaviour specific to the human species and its social structure.

In 2004, the team of Pier Vincenzo Piazza showed that the behaviours which define addiction in humans, also appear in some rats which will self administer cocaine. Addiction exhibits astonishing similarities in men and rodents, in particular the fact that only a small number of consumers (humans or rodents) develop a drug addiction. The study of drug dependent behaviour in this mammal model thus opened the way to the study of the biology of addiction.

Today, thanks to a fruitful collaboration, the teams of Pier Vincenzo Piazza and Olivier Manzoni are reporting discovery of the first known biological mechanisms for the transition from regular but controlled drug taking to a genuine addiction to cocaine, characterised by a loss of control over drug consumption.

Chronic exposure to drugs causes many modifications to the physiology of the brain. And researchers wanted to find out which of these modifications is responsible for the development of an addiction.
The addiction model developed in Bordeaux provides a unique tool to answer this question. Thus it allows comparing animals who took identical quantities of drugs, but of which only few become addicted.

By comparing addict and non-addict animals at various time points during their history of drug taking, the teams of Pier Vincenzo Piazza and Olivier Manzoni have demonstrated that the animals which developed an addiction to cocaine exhibit a permanent loss of the capacity to produce a form of plasticity known as long-term depression (or LTD).

LTD refers to the ability of the synapses (the region of communication between neurons) to reduce their activity under the effect of certain stimulations. It plays a major role in the ability to develop new memory traces and, consequently, to demonstrate flexible behaviour.

After short-term usage of cocaine, LTD is not modified. However, after a longer use, a significant LTD deficit appears in all users. Without this form of plasticity, which allows new learning to occur, behaviour with regard to the drug becomes more and more rigid, opening the door to development of a compulsive consumption.

The brain of the majority of users is able to produce the biological adaptations which allow to counteract the effects of the drug and to recover a normal LTD.
By contrast, the anaplasticity (or lack of plasticity) exhibited by the addicts leaves them without defences and hence the LTD deficit provoked by the drug becomes chronic.

This permanent absence of synaptic plasticity would explain why drug seeking behaviour becomes resistant to environmental constraints (difficulty in procuring the substance, adverse consequences of taking the drug on health, social life, etc.) and consequently more and more compulsive. Gradually, control of the taking of the drug is lost and addiction appears.

For Pier-Vincenzo Piazza and his collaborators, these discoveries also have important implications for developing new treatment of addiction.

“We are probably not going to find new therapies by trying to understand the modifications caused by a drug in the brains of drug addicts,” explain the researchers, “since their brain is anaplastic.” For the authors, “The results of this work show that it is in the brain of the non-addicted users that we will probably find the key to a true addiction therapy.

Indeed,” the authors estimate, “understanding the biological mechanisms which enable adaptation to the drug and which help the user to maintain a controlled consumption could provide us with the tools to combat the anaplastic state that leads to addiction”. (ANI)

Researchers have found that a specific and remarkably small fragment of RNA appears to protect rats against cocaine addiction – and may also protect humans.
The discovery could lead to better ways of predicting drug abuse risk and treating addictions

In the study, researchers at The Scripps Research Institute in Jupiter, Florida found that cocaine consumption increased levels of a specific microRNA sequence in the brains of rats, named microRNA-212.

As its levels increased, the rats exhibited a growing dislike for cocaine, ultimately controlling how much they consumed.
On the other hand, as levels of microRNA-212 decreased, the rats consumed more cocaine and became the rat equivalent of compulsive users.

The study’s findings suggest that microRNA-212 plays a pivotal role in regulating cocaine intake in rats and perhaps in vulnerability to addiction.
Interestingly, the same microRNA-212 identified in this study, is also expressed in the human’s dorsal striatum, a brain region that has been linked to drug abuse and habit formation.

“This study enhances our understanding of how brain mechanisms, at their most fundamental levels, may contribute to cocaine addiction vulnerability or resistance to it,” Nature quoted National Institute on Drug Abuse (NIDA) Director Dr. Nora D. Volkow, as saying.

“This research provides a wonderful example of how basic science discoveries are critical to the development of new medical treatments and targeted prevention,” he added.

Rats with a history of extended cocaine access can demonstrate behavior similar to that observed in humans who are dependent on the drug.
Current data show that about 15 percent of people who use cocaine become addicted to it.
The findings suggest that microRNAs may be important factors
contributing to this vulnerability.

“The results of this study offer promise for the development of a totally new class of anti-addiction medications. Because we are beginning to map out how this specific microRNA works, we may be able to develop new compounds to manipulate the levels of microRNA-212 therapeutically with exquisite specificity, opening the possibility of new treatments for drug addiction,” said Paul J. Kenny, senior author on the study.
The study is published in the journal Nature. (ANI)

“This report summarises the key findings from a report exploring public attitudes towards illegal drugs and drug misuse in Scotland, based on data from the 2009 Scottish Social Attitudes survey. It focuses in particular on attitudes towards opiate misuse, and on views of potential policy responses to this. However, it also places such attitudes in the context of wider views and experiences of illegal drugs.”

Main Findings
■ Support for legalising cannabis – which increased in Scotland (as in the rest of the UK) in the late 1990s – has fallen considerably in more recent years, from 37% in 2001 to 24% in 2009. Attitudes towards prosecution for possession of cannabis for personal use also hardened between 2001 and 2009.

■ Most people said taking cocaine occasionally is wrong – 76% rated it as 4 or 5 on a scale where 5 meant ‘very seriously wrong’.

■ 45% of people agreed that ‘Most people who end up addicted to heroin have only themselves to blame’, while just 27% disagreed.

■ Among those in paid employment, around half (47%) said they would be ‘very’ or ‘fairly comfortable’ working alongside someone they knew had used heroin in the past, while around 1 in 5 would be uncomfortable.

■ Just a quarter (26%) said they would be comfortable with someone who was receiving help to stop using heroin moving near to them, while half (49%) would be uncomfortable.

■ There was no public consensus on what should be the top government priority for tackling heroin use in Scotland – 32% chose ‘tougher penalties for those who take heroin’, 32% ‘more help for people who want to stop using heroin’ and 28% ‘more education about drugs’.

■ Just 16% agreed that people who possess heroin for personal use should not be prosecuted (compared with 34% for cannabis).

■ Public support for providing clean needles to injecting drug users fell from 62% in 2001 to 50% in 2009.

■ Opinion on educating young people about safer drug use was split – 44% agreed that young people should be given information about how to use drugs more safely, but 40% disagreed.

■ Four out of five (80%) agreed that ‘the only real way of helping drug addicts is to get them to stop using drugs altogether’. However, 29% agreed that ‘most heroin users can never stop using drugs completely’, while 27% said they neither agreed nor disagreed or did not know.

■ 63% disagreed that ‘Someone who has been a heroin addict can never make a good parent, even if their drug problems are in the past’.

■ Around two thirds (64%) said that young children of heroin users should be placed into temporary foster care until the parents stop taking heroin. A further 1 in 5 believed the child should stay at home while the family receives help from social workers and just 8% said the child should be permanently adopted by another family.

MULTIPLE DRUG USE NOW THE NORM, HEROIN SHUNNED BY YOUNG
Government drug policy is too centred on heroin abuse, fails to take account of the realities of current usage trends and needs to focus on individual user behaviour if it is to reflect the true picture and formulate meaningful responses, a leading academic at National University of Ireland Maynooth urged.
‘A Dizzying Array of Substances; An Ethnographic Study of Drug Use in the Canal Communities’ is the result of a long-term study which closely examined the realities of drug use in local life of Rialto, Bluebell and Inchicore, three communities served by the Canal Communities Local Drugs Task Force. It was led by principal investigator Dr A Jamie Saris and primary field researcher Fiona O’Reilly at the Department of Anthropology, NUI Maynooth.
The ethnographic research, carried out mostly in 2008 and early 2009, gives the most compelling evidence to date that multiple drug use is the norm amongst drug users in the Canal Communities and, the researchers concluded, most probably in other areas.
“The big problem is that as far as government is concerned, ‘drugs’, from a treatment perspective, has traditionally meant heroin. Thus, the apparent leveling off of the need for a very opiate-centric treatment service in the Canal Communities in recent years is deceptive” said Dr Saris.
Besides the ethnographic work, the study surveyed, on a long term basis, 92 people using either heroin or methadone in the study area. Unsurprisingly most of those surveyed were on methadone (98%). Of those surveyed:
•63% claimed to have used heroin in the previous three months
•30% had used crack cocaine
•22% had used powder cocaine
•46% had also taken street tranquilisers
•50% were on prescribed tranquillisers, and
•60% had also smoked cannabis within the past three months.
“The majority of those registered on the methadone treatment programme are also using a cocktail of other substances, very often including heroin. Multiple drug use is the reality for nearly all users, and official policy needs to have this understanding at its centre”, Saris said.
In the course of their study, the research team also noted a strong stigma against heroin use amongst the 16-25 age group who still regularly used a lot of other substances, including cocaine and off-label prescription medication. “The reality is that these people are difficult for a treatment infrastructure built around opiates to service. If they have issues, they are more difficult to address,” said Saris.
” The stress that policy-makers and community activists place on ‘crack’ or ‘heroin’ or any other single drug as clear and present social dangers obscures the ubiquity of polydrug use. It makes it appear that these users are very different from other drug-users in the rest of society including cannabis and recreational cocaine users, and it also obscures how commonly legal pharmaceuticals, such as benzodiazepines, even methadone itself, are regularly consumed ‘illegally’.”
He said that a focus on drug use alone is the mistake. “The lives we examined, however damaged by an attraction to certain pharmaceuticals, are rarely defined solely by such behaviour. These people are also sons and daughters, fathers and mothers, partners and lovers, as well as employees and community members. This sensibility does in fact inform a lot of local community activities aimed at assisting users, but such work is often difficult to justify to official funders under the rubric of ‘treatment’, as currently understood. Unless we can understand who users are, what they are taking and why, we will not be able to assign the appropriate resources, treatments or management systems.”
Tony MacCarthaigh, chairperson of the Canal Communities Local Drugs Task Force commented that “individuals and not chemicals need to become the focal point of treatment, and treatment needs to assist individuals in developing another orientation not just to drugs, but to life”.
Source: www.addictiontoday.org 9th July 2010

A DECISION by the Dutch government to decriminalise the smuggling of hard drugs could leave Britain vulnerable to a flood of cheap cocaine.
Customs officers are allowing traffickers caught at Schiphol airport, Amsterdam, with less than 3kg of cocaine to go free. The only penalty they face is the confiscation of their drugs.

In the first phase of a policy that could soon be extended to other hard drugs, the liberal measures are being applied to 35 so-called “cocaine flights” a week from the Caribbean.
Last year police caught 2,176 smugglers from the region and seized six tons of the drug. But from now on, traffickers no longer have to worry about hefty prison terms or even arrest.
The policy may prove even more controversial than Holland’s infamous “coffee shops”, where soft drugs such as cannabis have been sold openly for decades.
The Dutch authorities claim the measure will allow them to divert money spent prosecuting offenders into drug seizures. However, critics in neighbouring countries, including Britain, fear it will lead to a boom in the number of people ready to act as “mules” for drug cartels.
The National Drug Prevention Alliance in Britain has warned that the policy amounts to a capitulation by the police with consequences that could spin out of control.
“This won’t just hit the UK badly. It will affect the whole of Europe,” said David Raynes, a former chief narcotics investigator for Customs and Excise. “Holland is the drugs warehouse of Europe and by not controlling its problem it’s creating an infection that will spread to all the countries around.”
In Germany the street value of cocaine has already fallen from €150 (£102) a gram to just €50 (£34), raising the prospect of a sharp rise in the number of addicts. The Dutch government has ignored a plea from Otto Schily, the German interior minister, to toughen rather than weaken its deterrent.
However, Ivo Hommes, a spokesman for the Dutch justice ministry, said the initiative could save millions spent on prosecuting and jailing offenders, allowing more funds to go into the detection and confiscation of drugs. “Locking up thousands of smugglers doesn’t solve the problem. There will always be more of them,” he said. “We’ve been honest enough to admit that we only manage to stop 15% of the drugs coming in, so we are trying something new.”
A leaked ministry memorandum, however, has suggested that the policy was adopted because the prosecution service was overburdened. It emphasised that drug-related arrests should not be permitted to “block the justice system”. Britain’s National Criminal Intelligence Service is said to be eyeing the policy “warily”.
Source: February 01, 2004 The Sunday Times

Two Genes May Fuel Cocaine Addiction
Removing them caused withdrawal symptoms in mice
— Two related genes that help control signaling between brain cells may play an important role in cocaine addiction, says a study in the Aug. 5 issue of Neuron.
In research with mice, scientists found that deleting either of the two genes in the “Homer” family caused symptoms similar to those of cocaine withdrawal. The finding provides a new research target for trying to understand how both a genetic susceptibility to addiction and environmental factors cause addiction.
The study found the Homer1 and Homer2 genes appear to be specific for cocaine. When the researchers tested the effects of caffeine and heroin on mice that lacked the Homer genes, the rodents’ behavioral responses weren’t the same as they were with cocaine.
“While it can be anticipated that additional genetic models may be discovered that mimic or block behaviors associated with cocaine addiction, the striking concordant neurochemical phenotype between Homer2 deletion and withdrawal from chronic cocaine treatment indicates that Homer is a particularly good candidate to play a central role in cocaine addiction,” the study authors wrote.

A recent study by investigators at the Vanderbilt Kennedy Center for Research on Human Development may help explain the long-term behavioral and neurological problems associated with prenatal exposure to cocaine. In a recent issue of the Journal of Neuroscience, Gregg Stanwood, Ph.D., and Pat Levitt, Ph.D., report that prenatal cocaine exposure in rabbits causes a long lasting displacement of dopamine receptors in certain brain cells, which alters their ability to function normally.
Though this effect has not yet been assessed in cocaine-exposed children, the findings give researchers a place to start looking.
“The hysteria surrounding the ‘crack baby’ was sort of overblown,” said Stanwood, research assistant professor of Pharmacology and lead author on the study.
Incredibly high levels of cocaine — usually coupled with the abuse of other drugs — can lead to premature labor, preterm birth and low birth weight, Stanwood said.
“But in women who have abused relatively low recreational doses of cocaine, it is actually very hard to distinguish those children at birth from children born to anyone else,” he said. “However, as those children age, they do develop deficits in their cognitive and emotional development.”
These children often exhibit attention and arousal problems, similar to children with attention deficit hyperactivity disorder (ADHD). However, the standard treatments for ADHD — Ritalin and other stimulants — are not always effective in these children.
Studying the effects of prenatal cocaine exposure on the developing brain is difficult in human populations because cocaine abusers often abuse other drugs. Animal models can help determine how prenatal cocaine exposure might influence brain development to cause these subtle cognitive impairments.
“We thought that it was important to set up an animal model that recapitulates a key feature of human abuse — that being intravenous exposure to low doses of cocaine,” Stanwood said.
A few years ago, Stanwood and Levitt, professor of Pharmacology and director of the Vanderbilt Kennedy Center, established such a model in rabbits. They found that exposure to low levels of intravenous cocaine during a very short window of time during gestation — equivalent to the late first trimester and early second trimester in humans — caused specific alterations in brain circuits that use the neurotransmitter dopamine. Additionally, these cocaine-exposed offspring showed attention problems as well as insensitivity to stimulants like amphetamine, suggesting that cocaine exposure had altered the development of the dopamine pathways in the brain.
“In collaboration with Dr. Eitan Friedman of the City University of New York, we had previously shown a decrease in signaling of a particular receptor protein, the dopamine D1 receptor,” Stanwood said. “We know that this receptor is involved in regulating the formation of cortical circuitry. It’s also involved in the behavioral effects of amphetamines and cocaine.”
“The current study was an attempt to look at the mechanism of this decrease in D1 receptor signaling,” he said.
Stanwood examined the levels of D1 receptor in brain cells taken from “teenage” rabbits that were exposed to cocaine during that short, sensitive prenatal period.
He found that cocaine exposure did not alter the total amount of D1 receptor produced in the brain. However, there was a dramatic alteration in the location of the protein within the cell.
“It’s not where it should be,” he said. D1 receptors are normally found at the cell surface, but neurons from the cocaine-exposed animals showed the receptor was predominantly sequestered inside the cells.
“The fascinating thing is that this effect appears permanent,” said Stanwood. This implies that cocaine exposure during a brief, sensitive period of neural development can lead to long-lasting effects at the cellular level.
This change also altered the growth of neuronal processes, suggesting that the altered D1 receptor trafficking may underlie the changes in neuronal architecture and behavior that Stanwood and others have previously observed.
What remains to be determined, he cautioned, is whether D1 receptor localization is affected in humans exposed to cocaine prenatally.
If found in humans, “it gives us a new way to think about helping those children as they continue to mature.” Because cocaine exposure seems to alter the distribution of the D1 receptor, Stanwood suggests that researchers might find a way to “steer” the receptor into the correct cellular location. That could provide new avenues for treating the attention problems in cocaine-exposed children, as well as in children with stimulant-resistant ADHD.
“Neither we nor anyone else has yet identified whether this mechanism occurs in the human population,” Stanwood said, “so that is a critical next step.”
Note: This story has been adapted from a news release issued by Vanderbilt University Medical Center.

NIDA-supported researchers Dr. Cheryl Kirstein and Ms. Kirstie Stansfield at the University of South Florida have found that higher scores on tests of impulsivity and some behavioral responses to novelty correlate with a heightened biological response to cocaine in adolescent, but not adult, rats. The findings accord well with scientists’ widely shared view that developmental differences in brain systems that use the neurotransmitter dopamine underlie age differences in susceptibility to drug abuse.
Dr. Kirstein and Ms. Stansfield conducted a series of behavioral assays to rate rats’ relative responsiveness to novelty, then compared these results with measures of dopamine release in the reward pathway after an injection of cocaine. First, they put adolescent rats (34 days old, which is roughly equivalent to adolescence in people) and fully mature rats (59 days old, equivalent to human young adulthood) through four behavioral protocols. The tests measured activity in a new environment (how much the rat moved around when put into a new cage); impulsivity (how quickly it approached a new object placed into its cage); exploratory drive in response to a new object (how many times it approached the object in a given period of time); and attraction to new objects (what percentage of a given time interval was spent close to the object).
The researchers then injected the animals with saline and then, 2 hours later, with cocaine 20 mg/kg. Every 10 minutes, starting immediately after the saline injection and continuing until 2 hours after administering the cocaine, they measured the concentrations of the neurotransmitter dopamine and its major metabolite in the rats’ nucleus accumbens (NAc). The measurements were made using the technique of in vivo microdialysis. By the time of the last measurement, the drug had cleared the animal’s system.
ON MOST TESTS, AGE MATTERS
In their analysis, the researchers compared cocaine-induced dopamine release in animals that had responded above the mean level on each test (high responders, HR) to those who had scored below the mean (low responders, LR). The results revealed that among both the adult and adolescent rats, those that exhibited greater activity in a new environment also demonstrated enhanced dopamine release following a cocaine injection. This was the only test, however, in which age did not influence cocaine-induced dopamine release. The other behavioral assays revealed interactions between age and the response to novelty on cocaine-induced dopamine release in the NAc:
• Impulsivity—Adolescent rats with above-the-mean impulsivity scores released more dopamine in response to cocaine than their age mates who were LR. Mature rats exhibited no clear relationship between impulsivity and cocaine-induced dopamine response.
• Exploration of a new object—Adolescent rats with above-the-mean scores on this measure released more dopamine in response to cocaine than their age mates who were LR. Adult rats showed the opposite pattern: Animals with above-the-mean scores showed attenuated cocaine-induced dopamine release compared with age mates who were LR.
• Attraction to a new object—Adolescent rats exhibited no clear relationship between reactivity on this assay and cocaine-induced dopamine release. Mature rats with above-the-mean scores released less dopamine in response to cocaine compared with their age mates who were LR.
Dr. Kirstein’s finding that for all the animals, greater activity in a new environment corresponded with increased sensitivity to stimulants is consistent with earlier research. Her team’s mixed findings on the impulsivity and other novelty response tests indicates, she says, that those behaviors arise from different physiological mechanisms than does locomotor activity. “My colleagues and I think locomotor activity may reflect primarily dopamine activity in a brain circuit involved with generating and controlling movement. Novelty may instead differentially stimulate mesolimbic dopamine—a pathway implicated in attention as well as reward and motivation,” says Dr. Kirstein.
In Vivo Microdialysis
The investigators used In Vivo microdialysis to measure dopamine each animal released from its nucleus accumbens (NAc) in response to cocaine. They implanted a probe into the shell area of the NAc. The probe is a fine tube, about the size of a sewing needle, connected to a mini-pump that continuously perfuses it with artificial cerebrospinal fluid. The membrane tip of the probe captures dopamine and its metabolites. The samples collected by the needle are then analyzed using techniques, such as chromatography, that are able to isolate dopamine and its metabolites from other molecules.
INHIBITION DEVELOPS LATER
The findings on the three tests where age affected the relationship between behavior and cocaine-induced dopamine release may reflect maturation of the brain’s reward circuit. When rats are adolescents, dopamine-producing and releasing cells in this circuit may be particularly sensitive both to novelty and to pharmacological stimulation. As part of normal neurological development, areas of the brain that dampen the activity of this circuit come “online” later, explaining the age-related differences observed in Dr. Kirstein’s study. “The mesolimbic pathway and the cortical areas that inhibit it to regulate dopamine release are not yet fully matured in the adolescent, and this may explain why the adolescent brain responds to drugs differently than the adult brain,” says Dr. Kirstein.
“The results of Dr. Kirstein’s study, along with other animal research on the interaction of drugs and developmental stage, indicate that the adolescent brain is more responsive to drugs than the adult brain—both neurochemically and behaviorally,” says Dr. Nancy Pilotte of NIDA’s Division of Basic Neuroscience and Behavioral Research. Studies that identify the physiological and behavioral processes underlying age-related susceptibility to addiction complement epidemiological work on the individual and social factors contributing to adolescent vulnerability to substance abuse.

The annual United Nations World Drug Report published yesterday confirmed my analysis of the available data which shows the UK to have the worst drugs problem in Europe. Yet a month ago when the The Phoney War on Drugs was published by the CPS Jacqui Smith and the Home Office went into denial mode.
While repeating Labour’s worn out justification that “overall drug use is lower than when Labour took office”, and that this is “a clear sign that our strategy is working” – exactly the myth that my paper debunked – she resolutely turned her back on the facts of rising drug deaths, rising ‘problem’ drug use (now put by the UN at 400,000, some 70,000 higher than 2006 measures) rising prescribed methadone dependency and the doubling of cocaine consumption.
Even before the latest UN report figures were released new data in the last month on drugs related damage and a new analyses of seizure data confirmed my thesis. The Independent on Sunday revealed a 67% increase in the number of babies born suffering from drug withdrawal symptoms in the past 10 years even though these statistics (of opiate addicted babies) exclude those newborns with problems due to their mother’s exposure to cocaine, amphetamines and cannabis.
Yesterday’s UN Report repeated my comparative data analysis which showed that the UK is the largest market for cocaine and that consumption has more than doubled in recent years and is higher than anywhere else in Europe.
Martin Blakebrough, the CEO of the drug charity Kaleidoscope said in response that, “The numbers exploded probably around five years ago and they’ve continued to rise because it’s become more mainstream .. it has a kudos or glamour not associated with other substances”. Meanwhile drugs counsellors confirm that teenagers are moving from cannabis to cocaine as young as 14 and that use by children as young as 11 is rising. It is something that the government’s preferred treatment intervention, methadone prescribing, can do nothing about.
SOCA’s claim that this consumption rise is despite cocaine prices reaching record levels due to their interdiction must however be treated with extreme scepticism. These are not street prices and reflect currency exchange rate changes as I pointed out a few weeks ago.
The truth is that the explosion in cocaine use mirrors a period in which UK cocaine quantity seizures have dropped, as have prices, while the market has expanded. The hard evidence I detailed in my paper points to failing enforcement competence and commitment on the part of the government and SOCA. Furthermore publication this month of an analysis of Scottish heroin seizures by Professor Neil McKeagney confirmed that these are at record lows.
So, surely now the Government and its various drugs satellites and quangos must face the truth of the uniquely appalling social problem we face in Britain and the extent to which their misguided policy has contributed to it. They must finally give up trying to justify themselves by one selective measure of drugs use prevalence picked from the British Crime Survey and the English Schools survey and accept the fact that this does not even begin to measure the extent of drugs related harm. Even less does it measure policy efficacy.
Nowhere is this claim less credible than in their resort to these ‘official’ measures of declining cannabis use to ‘prove’ that adolescent drug use and addiction are under control. Neither of these surveys reach the part of the population that drugs reach most. Fewer schools sampled each year chose to cooperate. The number of truanting, absentee and excluded children continues to rise. The Government apparently remains convinced that if schoolchildren’s cannabis use is dropping that this is sufficient unto the day. The ‘if’ remains quite big.
The reality on the streets however is one of a youth alcohol and drugs crisis that Ray Lewis illustrated powerfully in response to my paper. The number in need of drugs treatment continues to rise (alongside hospital admissions); demand outpaces provision while the ‘treatment’ on offer is totally inadequate.
One thin and poorly nourished boy I met last week told me that on his estate he knew no one, neither adolescent nor adult, who did not use drugs. And just a few weeks ago when I asked a health visitor working in inner London how many of the 400 families on her books had a drug problem, she countered defensively, “don’t ask, it is a fact of life, we have to accept it.” That is the trouble. This is the official attitude to drug use and everything that goes with it is: ‘There is nothing you can do’.
But it is the Government’s performance-driven, methadone ‘treatment’ drugs policy that is maintaining these lifestyles rather than changing them. All the kids do, one adolescent addiction counsellor told me, is use ‘community treatment’ on offer as part of this lifestyle. They are offered nothing to make them change or to enable such a change. Treatment ‘in the community’ leaves them with the same older adults still in their lives and subject to the same environment. They may go through several methadone ‘detoxes’ with the aim of ‘bringing down’ their illicit drug use, but this is often even without a plan to reduce the methadone use. There is no other ambition. “You can get up to 40mls of methadone a day if you are under 16”, one girl confidently told me. “All it does”, she said, “is to keep everything going – to maintain everything else”.
She was one of the handful of lucky ones. Two three month sessions at Middlegate, the only dedicated residential adolescent addiction centre in the country, had changed her life. A heroin addict at 14, moved from one inadequate foster home to another, finding herself on the street and in dealers flats, missing out on years of her education, she had, thanks to one enlightened and persistent social worker who forced the local authority to stump up the cash, been sent to Middlegate. This summer she has been sitting four academic AS levels.
The staff at Middlegate despair at the years of wasted public money pumped into ‘community treatment’ when they know what they can achieve with the most desperate of cases. What the kids need, they say, is rescuing and lifting out of their environments – not a sequence of social workers and drug workers operating with their government defined agendas to ‘rebuild families’ at whatever the cost yet incapable of providing the long term commitment required.
Yet the National Treatment Agency, wedded to this ‘treatment in the community’ agenda for all adolescents, refuses to ring fence any funds for Middlegate to ensure this life changing programme can continue, let alone be replicated anywhere else.
Responding to The Phoney War on Drugs one highly respected addiction psychiatrist commented that I had not emphasised sufficiently “the huge waste of resource brought about by the NTA’s enthusiasm to allow managerialism to take over the field.” He is right. The NTA’s approach to treatment is now so entrenched in a complex, resource hungry but inflexible bureaucracy that it is standing in the way of the revolution in rehabilitation that is required. Nothing less than a major diversion of resources in the direction of rehabilitation and away from people processing plus a clearly conditional and contractual approach to drug treatment will work.
The government would do well now, before inflicting more damage on our society, to face the facts and acknowledge that their approach to ‘treatment’ and their drugs policy has failed abysmally.
Source: http://www.cps.org.uk 25.06.2009

More than 11,000 children under 16 years old were treated last year for addictions to alcohol and drugs, including heroin, according to new figures released this week.
The National Treatment Agency for Substance Misuse puts the total figure of children treated at 11,294. This includes 6,075 under-16s addicted to cannabis, of which 102 are under 12 years old.
More than 4,000 children received help for alcoholism, including 57 under-12s.
The children addicted to class A drugs included ten under-12s who were dependent on heroin, out of 93 under-16s. A further 323 children were treated for cocaine misuse, 165 for ecstasy, and 36 for crack.
Conservative Health Secretary Andrew Lansley said the government is neglecting a ‘forgotten generation’ of children. “It’s a sad indictment of our broken society that so many are turning to things like drug and alcohol abuse at such a young age” he said.
The Department of Health said the high figures were due to an increase in spending on treatment, a rise of £10million, from £15million to £25million in the past five years,
Funding for the government’s national anti-drug campaign which is aimed at teenagers has been cut by 41 per cent from £9.05million in 2006-7 to £5.35million today.
Charity Drugscope offered an optimistic approach to the figures, saying the overall numbers of young people using illegal drugs has fallen in recent years, especially cannabis.
Source: www.askamum.co.uk 8th July 2009

Research Summary
Cocaine and amphetamine users appear to develop an abnormal protein in their brains that could play a role in addiction.
Researchers at the Rosalind Franklin University of Medicine and Science in North Chicago, Ill., found that use of these drugs alters a protein that controls how RNA is copied — an anomaly that could cause structural changes in tissues, diseases, and behavior changes.

Reference:
Marinescu V, Loomis PA, Ehmann S, Beales M, Potashkin JA (2007) Regulation of Retention of FosB Intron 4 by PTB. PLoS ONE, 2(9): e828; doi: 10.1371/journal.pone.0000828.
This article summarizes a mainstream media report of research published in a scientific journal. It is not an original analysis of the source material, which is cited in the reference above.

In a study published today in the journal Addiction, researchers in the United States have discovered that accidental overdose deaths involving cocaine rise when the average weekly ambient temperature passes 24 degrees Celsius (75 degrees Fahrenheit). Using mortality data from New York City’s Office of the Chief Medical Examiner for 1990 through 2006, and temperature data from the National Oceanic and Atmospheric Association, researchers found that accidental overdose deaths that were wholly or partly attributable to cocaine use rose significantly as the weekly ambient temperature passed 24 degrees Celsius. The number of cocaine-related overdose deaths continued to rise as temperatures continued to climb.
Cocaine-related overdose deaths increase as the ambient temperature rises because cocaine increases the core body temperature, impairs the cardiovascular system’s ability to cool the body, and decreases the sense of heat-related discomfort that ordinarily motivates people to avoid becoming overheated. Cocaine users who become overheated (hyperthermic) can overdose on lower amounts of cocaine because their bodies are under more stress.
The study’s findings correct previous research that associated an increase in cocaine-related mortality with much higher temperatures (31.1 degrees Celsius, or 87.9 degrees Fahrenheit). Because cocaine-related overdose fatalities begin to rise at lower ambient temperatures than was previously thought, it is now apparent that cocaine users are at risk for longer periods of each year. Between 1990 and 2006, the average weekly temperature in New York City rose above 24 degrees Celsius for about seven weeks per year.
The study showed no difference in the number of drug overdoses in New York City among those weeks where the average temperature was between -10 and 24 degrees Celsius. Above 24 degrees Celsius, however, there were 0.25 more drug overdoses per 1,000,000 residents per week for every two degrees increase in weekly average temperature. Given that over 8.2 million people live in New York City, the study’s findings predict that at least two more people per week will die of a drug overdose in the city for each two degree rise in temperature above 24 degrees Celsius, compared to weeks with average temperatures of 24 degrees and below.
The authors of this study point out the need for public health interventions in warm weather, such as delivering health-related warnings to high-risk groups. Prevention efforts could also include making air conditioning available in locations where cocaine use is common such as urban areas with a known high prevalence of cocaine use, and within those urban areas, particular neighbourhoods with elevated numbers of cocaine-related deaths or arrests. As lead author Dr. Amy Bohnert explains, “Cocaine users are at a high risk for a number of negative health outcomes and need public health attention, particularly when the weather is warm.”

According to details given by the NHS, there has been a 65 per cent increase in people receiving treatment for cocaine addiction in UK. These are teenagers which is cause of concern.
These figures correspond to the announcement by the Advisory Council on the Misuse of Drugs (ACMD) earlier. It was found by an NHS study, conducted by the National Treatment Agency for Substance Misuse, that the number these teenagers has doubled since 2005.
It was reported that users were combining cocaine with alcohol that causes more damage to the heart and makes users more violent. It was noticed that a six-month treatment treated four in 10 people and they were no longer addicted, but several left the treatment midway.
In England, about 12,354 people were treated for cocaine addiction last year. Between 2005-06 and 2008-09 a rise was seen in the number of people coming for treatment and the figures increased from 453 to 745, and the number of 18- to 24-year-olds doubled from 1,586 to 3,005.
The chairman of the ACMD, Professor Les Iversen stated, “The figures were deeply concerning.”
The Conservatives and Liberal Democrats both stated that a change was needed in the government’s approach to tackling addiction.

The recreational use of cocaine has rapidly increased in many European countries over the past few years. One cause of this is the fall in the price of the drug on the street from 100 Euros for one gram (about 5 lines) in 2000 to 50 Euros in the Netherlands today. One line of cocaine is, thus, now as cheap as a tablet of ecstasy. This means cocaine is no longer considered an “elite” drug but is affordable for all, especially for recreational use. It is therefore likely that the recreational use of cocaine will become a public health issue in the next few years, which is already the case for the recreational use of ecstasy.
In a study in PLoS One, researchers at Leiden University and the University of Amsterdam, led by Lorenza Colzato, employed the “stop-signal paradigm” to measure the length of time taken by subjects to initiate and suppress a prepared reaction.
The stop-signal task requires participants to react quickly and accurately by pressing a left or right key in response to the direction of a left- or right-pointing green arrow. In 30% of the trials, the green arrow turned red, in which case participants had to abort the go response. The results show that while both recreational users of cocaine and non-users performed similarly in terms of response initiation, users needed significantly more time to inhibit their responses.
The study is the first of its kind to investigate systematically action control, and the inhibitory control of unwanted response tendencies in particular, in recreational users, i.e. those who don’t meet the criteria for abuse or dependency but who take cocaine (usually by snorting) on a monthly basis (1 to 4 grams). The researchers found that the magnitude of the inhibitory deficit in recreational users was smaller than previously observed in chronic users, suggesting that the degree of the impairment is proportional to the level of cocaine use.
Given the seemingly small quantities of cocaine involved, the findings of this study are rather worrying. Many real-life situations require the active inhibition of pre-potent actions, as in the case of traffic lights turning red or of criminal actions. This impairment of inhibitory control has serious implications for personal or societal functioning. This reduced level of inhibitory control may even be involved in the emergence of addiction: the more a drug is used, the less able users are to prevent themselves from using it.

Source: Public Library of Science PLoS One 2(11): e1143.doi:10.1371/journal.pone.0001143 2007, November 7.

According to a new report from the National Treatment Agency for Substance Misuse (NTA), people aged 18 to 24 now account for a third of all those in England seeking treatment for cocaine addiction.
Last year, over 3,000 18 to 24-year-olds sought treatment for cocaine use, with another 745 users under the age of 18.
This is nearly double the number who sought treatment in 2005-2006.

Over 60% of all cocaine users seeking treatment remain abstinent six months after completing their treatment, the NTA says.
However, the most recent British Crime Survey estimates there are 437,000 people aged 16 to 24 in England and Wales who have used cocaine in the past year.
The survey says the number of 16 to 24-year-olds to have used cocaine in the past year rose from 5.1% to 6.6% – the highest percentage of users yet.
The Class A drug is no longer seen as the preserve of the celebrity classes and can be brought on most city streets for “pocket money” prices, starting as little as £15 a bag.
Only cannabis and alcohol are more popular, while the use of designer dance drugs like ecstasy is falling.
Tumbling prices and the lack of stigma attached to powder cocaine have also led to increasing use at every level of British society. The number of cocaine dealers is also mushrooming, with a proliferation of younger street-level dealers who are known in urban slang as “shottas”.
Drugs education charities are warning that urgent action is needed so that recreational users are made aware of the dangers.
Cocaine is a class A drug that can cause anxiety, a rise in blood pressure and heart problems, as well as long-term addiction.
Statistics in a recent NTA report show that over 50% of cocaine users will also drink alcohol while using cocaine – a particular concern, as this creates a third highly toxic chemical in the body called cocaethylene, which can cause severe harm to the liver.
The potential health hazards are exacerbated by the fact that a lot of the cocaine sold on the streets is heavily adulterated, or “bashed”, as dealers refer to it, with various substances like crushed painkiller tablets and other stimulants.

Adding to the evidence that maternal drug use can have lasting effects, a new study finds that young schoolchildren of cocaine-using moms scored more poorly on attention tests.

Researchers looked at test scores of 415 African-American children who took tests at age 5 or 7 (now 14 to 16 years old). The mothers of 219 of the children had taken cocaine while pregnant, and the mothers of the other 196 had not. All of the mothers were poor and living in the Miami inner city.

Children born to cocaine-addicted moms showed signs of having more trouble paying attention than the other kids. They were more likely to make errors of omission and had slower reaction times on tasks.

“This study provides further evidence of a subtle but consistent effect on attention through early school-aged years,” said lead author Veronica Accornero, assistant professor of clinical pediatrics at the University of Miami.

However, the effects are minor, and one pediatric specialist suggested they pale next to the problems caused when mothers use alcohol and tobacco. In general, children born to cocaine-using mothers “are doing much better than anyone predicted, especially considering their background,” said Tamara Warner, research assistant professor at the University of Florida who is familiar with the study findings.

The study appears in the June issue of the Journal of Developmental and Behavioral Pediatrics.

During and after the crack epidemic of the 1980s, so-called “crack babies” were the subject of media coverage and concern about their futures. Researchers found, however, that the effects in general “appear to be more subtle and specific than initially believed,” Accornero said.

She said the children do not appear to have a hard time with “intellectual functioning,” although they might have difficulties with language, attention and behavior.

The future effects on these children is unclear. “Certainly, attention and the ability to maintain attention is an important skill that supports the development of other skills like language and behavior,” Accornero said. “It’s possible that because of subtle deficits we may see an effect on academic performance. We just don’t know yet.”

People with a certain gene variant appear to be at higher risk of cocaine addiction, according to researchers from the Institute of Psychiatry.
Medical News Today reported March 13 that some people have a gene that stops the production of DAT, which regulates removal of extra dopamine in the brain. Cocaine works by limiting DAT, overloading the brain with dopamine.
People who have the DAT-limiting gene were found to be more likely to become addicted to cocaine; those with two copies of the gene were at even higher risk.
“This study is the first large-scale search for a genetic variant influencing the risk of developing cocaine addiction or dependence,” said lead researcher Gerome Breen. “The target we investigated, DAT, is the single most important in the development of cocaine dependence. It made sense that variation within the gene encoding DAT would influence cocaine dependence.”Source: Proceedings of the National Academy of Sciences.March 2006

Long-term cocaine use can alter the function of genes in the brain, leaving “pleasure circuits” stuck in the open position and increasing craving for the drug, according to a new animal study conducted by researchers at the Mount Sinai School of Medicine.
Reuters reported Jan. 9 that researcher Ian Maze and colleagues found that the gene 9A — which produces an enzyme responsible for switching other genes on and off — was repressed in the brains of mice given repeated doses of cocaine. Researchers also found that restoring the activity of gene 9A reversed cocaine preference and craving in lab mice.
“This finding is opening up our understanding about how repeated drug use modifies in long-lasting ways the function of neurons,” said Nora Volkow, director of the National Institute on Drug Abuse.Source: Science. Jan. 8, 2010

Research Summary
Using electrical charges to stimulate the subthalmic nucleus region of the brain may mitigate cocaine addiction without disrupting the dopamine system like current anti-addiction medications, according to French researchers.
The Los Angeles Times reported Dec. 28 that researchers reported that deep brain stimulation performed on cocaine-addicted lab rats resulted in the rats exhibiting less self-administration of the drug than an untreated control group.
Researchers also found that the treated rats seemed to break the association with an area where cocaine had been distributed, preferring to instead linger in an area where food was provided.Source: Proceedings of the National Academy of Sciences (PDF). Dec.2009

ABSTRACT
The present study was conducted to determine whether methadone maintenance alters the pharmacodynamic effects of single doses of cocaine. Twenty-two current users of IV cocaine who were not seeking treatment for their illicit cocaine use participated while living on a research unit.
Eleven were maintained on methadone 50 mg PO daily as treatment for their opioid abuse; 11 were opioid abusers who were not physically dependent on opioids and who provided opioid-free urines throughout the study. Each subject received acute cocaine challenge doses of 0, 12.5, 25, and 50 mg intravenously in random order under double-blind conditions in separate test sessions.
Physiologic and subject-rated responses were measured before injection and for 2 h after. In the methadone maintenance group, cocaine challenge sessions occurred 15.5 h after the daily methadone dose. There were significant differences between the methadone-dependent and nondependent groups: 1) baseline differences related to chronic methadone administration and not associated with cocaine administration (lower respiration rates and pupil diameter; higher skin temperature) and 2) differences in response to cocaine administration; cocaine-induced increases in subject ratings of Drug Effect, Rush, Good Effects, Liking, and Desire for Cocaine and in heart rate were greater in the methadone maintenance patients compared to the non-dependent group.
These results indicate that the positive subjective effects and some physiological effects of cocaine are enhanced in methadone-maintained individuals, suggesting a pharmacological basis for the high rates of cocaine abuse among methadone maintenance patients.

The number of cocaine users being admitted to hospital has quadrupled in eight years, it has emerged as concerns grow that it has become the drug of choice for middle-class men.
An average of more than two people a day are admitted to accident and emergency units for “cocaine-induced health emergencies”, official Government data showed.
There were 740 incidents in 2006-07 compared with 161 in 1998-99.
The figures revealed that 85 per cent of the patients were men, with an average age of 29.
In comparison, heroin overdoses and cannabis poisonings both fell in the same period, according to the figures obtained by Druglink magazine.
The statistics expose the scale and impact of cocaine’s growing popularity and come after a series of high-profile cases involving the drug.
Recent drugs crime surveys have also reported growing use of cocaine among the urban middle classes. One study found one in three young men attending A&E at a London hospital with suspected heart attacks were cocaine users

Home Office figures show that use of the drug has more than doubled among 16 to 24-year-olds since the start of the decade, and Britain remains one of the countries with the highest level of cocaine abuse, along with Spain and Italy

ScienceDaily (Aug. 16, 2008) — A possible future way to prevent relapses into drug dependence has been discovered by researchers at Linköping University and the German cancer research center DKFZ. The target is the dopamine-producing nerve cells in the midbrain.Earlier research has shown that these cells become more excitable when a person takes drugs. To find out the functional meaning of this, these researchers used a mouse model for cocaine dependence. When they blocked the cells’ receptors for glutamate ¬- the brain’s most important signal substance -¬ the risk of relapsing into addiction vanished. The findings are being published in Neuron.
Dopamine-producing nerve cells are central to the brain’s reward system. Dependence-inducing drugs cause concentrations of dopamine to rise in the surroundings, which in turn affects other nerve cells and brings about various physical and mental reactions.
Cocaine has a very rapid impact on dopamine levels, which explains why it is one of the most addictive drugs.
“When you take cocaine, the number of glutamate receptors increases, rendering the cell more excitable. When we block this process, we prevent relapses into addiction. This is interesting clinically since that is the phase when we can get hold of patients,” says David Engblom, a neurobiologist at Linköping University and the study’s lead author.
An addict who wants to give up drugs could thus be offered a ‘vaccination’ against relapsing. But much more research remains to be done before such treatment can become a reality.

Research SummaryA brain imaging study conducted by researchers at Massachusetts General Hospital revealed that abnormalities appearing in the cerebral cortex of cocaine addicts correlate with dysfunction in regions of the brain responsible for attention and reward-based decision-making.
While some of these abnormalities may reflect a predisposition to drug use, others may result from long-term cocaine exposure. “These data point to a mixture of both drug effects and predisposition underlying the structural alterations we observed,” said Hans Breiter principal investigator of the Phenotype Genotype Project in Addiction and Mood Disorder.
Magnetic resonance imaging studies of 20 cocaine addicts and 20 control participants were used to determine variations in cortical thickness. Compared to the healthy controls, the cocaine addicts had significantly less overall cortical volume. The difference was markedly apparent in areas that control reward functioning and decision-making. In addition, typical differences in thickness in the frontal regions of the cortex was reversed for the addicts compared to non-addicts.
“The severity of these cortical alterations point to the potential importance of prevention efforts to keep susceptible individuals from beginning to use cocaine,” Breiter said. He suggested that further large-scale testing of individuals with different addictions is needed “to see if these findings are limited to cocaine users.”

Source The report appears in the Oct. 9, 2008 issue of the journal Neuron.

Middle-class women are in the grip of an alarming epidemic in cocaine use.
The number seeking NHS help for addiction to the Class A drug has leapt by 50 per cent in two years. Last year, some 2,923 women and girls sought help, according to the National Drug Treatment Monitoring System – the equivalent of eight every day.
Meanwhile, statistics released by the Ministry of Justice show that, since 2002, there has been an almost five-fold increase in the number of women cautioned by police for possession of cocaine. Outside of London, the affluent home counties of the Thames Valley, Hertfordshire and Sussex are the places where officers issue the most cautions for cocaine possession to women.
It will fuel fears the drug, in combination with alcohol, is taking a firm hold on the social lives of professional women who see it as ‘glamorous’.
DrugScope chief executive Martin Barnes said: ‘Cocaine was traditionally seen as a glamorous drug, usually associated with a wealthy or jet-set lifestyle. ‘While the drug has become cheaper and more available in the last decade, it has unfortunately kept some of this so-called glamorous image. ‘Cocaine is far from a safe or risk-free drug. Users can experience anxiety, insomnia and heart problems and the risks increase when the drug is combined with alcohol.’
Drug treatment experts said those seeking help for addiction to cocaine were professionals with well-paid jobs. Critics claim use of the drug has been promoted by high-profile celebrities who confess to taking it but avoid prosecution.
Kate Moss and Jodie Kidd have been exposed as users, while classical singer Katherine Jenkins and Amy Winehouse have confessed to taking the drug.
Adrian Rides, a drug addiction recovery expert for New Choices, said: ‘It is only in the last five years that cocaine has become as popular as it is and people are starting to get into trouble with it. Most of the people I work with are entrepreneurs, bankers, musicians – basically successful and dynamic people. ‘The people who get into trouble with cocaine are often successful small business managers and the drug taps into that drive.’
Figures obtained by the Mail under Freedom of Information laws show the number of women needing treatment for all drug addiction has risen from 50,462 in 2005/06 to almost 57,000 in 2007/08. This included 3,282 who were addicted to crack. The number of cautions given to women for cocaine offences has surged from 153 in 2002, to 542 in 2006, and 740 in 2007.
Among men the problems associated with cocaine are similarly bad. The number of NHS addicts needing treatment has soared from 6,371 in 2005/06 to 9,690 in 2007/08, an increase of 52 per cent.
Men being cautioned for possession of cocaine has also leapt – from 2,104 in 2004 to 6,634 in 2007. Cocaine was also the most commonly seized class A drug in 2006/07, with 16,079 seizures, up 35 per cent since 2005. It is the first year since records began in 1973 where cocaine seizures have totalled more than those of heroin.
Almost two in every three of the cocaine seizures were for amounts under one gram – indicating they were for use by the individual who had been caught rather than a dealer. Last year, it was estimated that 750,000 in the country had snorted cocaine in the previous 12 months. A report by the European Monitoring Centre for Drugs and Drug Addiction said young people in the UK were more likely to take cocaine than those in any other country on the continent.
One in 20 children of 15 and 16 have used the drug, it said.
The rise in use comes in the wake of evidence of increased binge-drinking among women, allied with a surge in their involvement in violent attacks.Source: Mail Online 26th Jan. 2009

ScienceDaily (Feb. 20, 2009) — An ingredient in licorice shows promise as an antidote for the toxic effects of cocaine abuse, including deadly overdoses of the highly addictive drug, researchers in Korea and Pennsylvania are reporting.
In the new study, Meeyul Hwang, Chae Ha Yang, and colleagues note that there is currently no effective medicine for treating cocaine abuse or addiction. Recent animal studies conducted by the researchers show that a licorice ingredient called isoliquiritigenin (ISL) can block the nervous system’s production of dopamine. That neurotransmitter is involved in emotion, movement, and other brain activities.
Cocaine and other addictive drugs stimulate dopamine and help produce the pleasurable and addictive effects. Drugs that block dopamine block this response. The scientists used rats as model animals to show that rats injected with ISL just prior to cocaine-administration showed 50 percent less of the behavioral effects associated with the illicit drug.
They also showed that ISL injections protected nerve cells in the brain from cocaine-associated damage.

Evidence has emerged which points to a link between cocaine use and violent behaviour in Britain’s city centres.
Figures from Greater Manchester Police suggest that 41% of people arrested for violence had taken cocaine or crack cocaine, by itself or with other drugs.
The force took samples from 1,000 people arrested for offences such as assault, wounding and affray in the seven months to March last year. The charity DrugScope revealed the results in its magazine, DrugLink.
The survey was part of an article which considered whether mixing alcohol and cocaine was a recipe for disaster.Similar findings had been reported in the Liverpool area after a separate study, run last summer by John Moores University.
Aggressive behaviour
Chief Inspector Dave Boon, who leads Greater Manchester Police’s drug intervention programme, said while only a small number of offenders had been tested so far, the statistics were important.

“We cannot afford to ignore the link between violence, drugs and alcohol that is apparent in city centres all over the UK every weekend,” he said.
“What this survey is doing is trying to prove that link and developing ways to manage the problem.”
DrugScope chief executive Martin Barnes said: “The investigation carried out by our magazine does suggest some link between powder cocaine use and violent and aggressive behaviour.
“However, because the drug is so often taken in combination with alcohol we need to be cautious about claims that cocaine alone can lead to violent offending.”
Cocaine is more widely used in Britain than ever, while the average price has halved in a decade. A wrap can cost as little as £25.
Further research will be conducted this year, with police keen to establish whether there is a link between alcohol, cocaine and domestic violence.

Research Summary
Cocaine use during pregnancy can cause cognitive impairments such as attention deficit, learning disabilities and emotional problems among children, according to researchers at the Vanderbilt Kennedy Center for Research on Human Development.
“The hysteria surrounding the ‘crack baby’ was sort of overblown,” said lead author Gregg Stanwood, Ph.D. “[I]n women who have abused relatively low recreational doses of cocaine, it is actually very hard to distinguish those children at birth from children born to anyone else. However, as those children age, they do develop deficits in their cognitive and emotional development.”
Animal studies conducted by Stanwood and co-author Pat Levitt, Ph.D., found that prenatal cocaine exposure resulted in a lingering and impairing shift in dopamine receptors in the brain. “We thought that it was important to set up an animal model that recapitulates a key feature of human abuse — that being intravenous exposure to low doses of cocaine,” Stanwood noted.
The study found that the location of D1 dopamine receptors appeared to be permanently altered in cocaine-exposed animals, suggesting that maternal cocaine use during a key period of neural development may have long-lasting effects.Source: Jan. 3, 2007 issue of the Journal of Neuroscience.

Research Summary
Young children of mothers who use cocaine scored somewhat worse than other children on tests designed to measure their attention, the Health Behavior News Service reported June 12.
The study of 415 African-American children ages 5-7 found that those born to mothers who used cocaine while pregnant did worse on the attention test, made more errors of omission, and reacted slower on tests. Differences between the cocaine group and other children were minor, however.
“This study provides further evidence of a subtle but consistent effect on attention through early school-aged years,” said study author Veronica Accornero of the University of Miami.
Still, the results were a far cry from the “crack baby” fears of the 1980s, and experts said that alcohol and tobacco use during pregnancy cause far greater problems.Source:June 2007 issue of the Journal of Developmental and Behavioral Pediatrics.

One in 15 women aged ten to 25 admit they have taken the drug after the proportion increased by a third in just three years. The sharp rise has sparked concerns that young women will soon overtake their male counterparts for cocaine use.
It echoes patterns seen with alcohol abuse where there has been a rise in women binge-drinkers and will further fuel evidence of a growing “ladette” culture.
Cocaine is seen as more socially acceptable and glamorous as high profile celebrities such as Kate Moss, Jodie Kidd and Amy Winehouse have been exposed for alleged involvement with the drug. Even opera singer Katherine Jenkins has admitted to taking cocaine a number of times several years ago but has since spoken out against drugs.
The pattern was revealed in a report on drug use in England for the Chief Medical Officer by the (National) Association of Public Health Observatories, published today.
Jim McVeigh, the co-author and an epidemiologist at Liverpool John Moores University, said: “We should not be surprised by these figures because we have seen the same thing happening with alcohol, which is intrinsically linked with cocaine.
“As women have become more and more prevalent in drinking environments they have been more exposed to cocaine which at the same time has also become more widely available and cheaper. “There is also not the same stigma attached to it as with some other drugs, it is more socially acceptable especially with celebrities helping to give it a glamorous image.
“There is also the feeling among women that they can take cocaine on an occasional social basis and not get hooked, but that of course is not necessarily the case with many ending up experiencing medical problems.”
Figures show in 2003 some 4.8 per cent of women aged ten to 25 in England admited to having tried cocaine while 8.2 per cent of men had. By 2006, 6.7 per cent of women in the same age group had taken cocaine while the proportion of men had fallen to 7.3 per cent.
Earlier this year the National Drug Treatment Monitoring System revealed the number of women seeking help for addiction to cocaine has doubled in two years.
Last year, 2,923 women and girls sought treatment for the Class A drug and the Ministry of Justice says since 2002 there has been a fivefold increase in the number of females cautioned for possession.
There are also added health risks because dealers often “cut” their cocaine with other, unknown chemicals to increase the amount that they can sell.
MPs were warned yesterday that a “new industry” is developing in the UK for cutting cocaine to reduce its purity.
Harry Shapiro, director of communications for the charity DrugScope, said pain killers are even being mixed in to give the same “numbing” effect to suggest the drug is stronger. But Mr Shapiro dismissed the suggestion that celebrity drug abuse influences youngsters as “ludicrous”.
He was giving evidence to the Commons Home Affairs Select Committee, where one Labour member appeared to attempt to smear senior Conservatives in a dig at Oxford University’s elite Bullingdon Club. Martin Salter asked the witnesses when cocaine had gone from being “the preserve of the Bullingdon Club and posh dinner parties to working class estates?”
Former members of the famous university social club include David Cameron, George Osbourne and Boris Johnson. Today’s report also reveals the rate of use across all ages who have admitted taking cocaine has increased overall, and substantially in most English regions between 2002/03 and 2007/08.
Regionally, about 47,000 crack cocaine users are estimated to live in London (2006/07), one and a half times more per 1,000 population (aged 15-64) than the national average. Overall, more deprived communities were associated with higher levels of problematic drug use and drug treatment than more affluent communities.
Sir Liam Donaldson, the Chief Medical Officer, said: “Drug misuse has a profound impact on health and wellbeing, affecting not only users, but their families and surrounding communities.”Source: Telegraph.co.uk 10th June 2009

Research SummaryResearchers from the Brookhaven National Laboratory and the National Institute on Drug Abuse (NIDA) have demonstrated that an area of the brain called the Anterior Cingulate Cortex (ACC) shows differences in levels of activity between cocaine users compared with non-users when performing a series of tasks, even though both groups are evenly matched demographically (socially, cognitively, educationally, etc.).
The study suggests that this difference in brain activity is not due to prior variance in cognitive ability or lack of motivation on the part of drug users, but rather because drug-users’ brains act differently from non-users’, Medical News Today reported May 26.
The researchers took 17 individuals with current cocaine-use disorders (CUD) and 17 demographically matched healthy controls and gave them several tasks to perform while the subjects underwent functional magnetic resonance imaging.
Both groups performed equally well at all the tasks. However, the levels of ACC activity differed between the two groups as the tasks were performed. In tasks that required monitoring behavior, activity in the ACC increased among the healthy non-drug users, but for the cocaine users this did not happen. Also, among the cocaine users the level of ACC activity was lowest in those who had used cocaine more frequently.
In other tasks in which emotion needs to be suppressed (emotion-monitoring), another part of the ACC becomes less active, but in the cocaine users this activity was not suppressed to the same extent as among non-drug users.
The major functions of the ACC (behavior-monitoring and emotion-monitoring) are located in a pair of regions in the same area of the brain. When the researchers measured the subjects’ responses to stimuli, these two regions of the brain behaved differently between the non-drug users and the drug users. Among the non-addicted subjects, the researchers found that the two parts of the ACC communicated with each other whereas among the cocaine users such communication did not take place. The researchers suggest that this was because the drug users experienced a disruption between the two functions of the ACC.
Lead author Rita Z. Goldstein, a psychologist at Brookhaven National Laboratories, said the study, “gives us some clues as to what happens when drug users are unable to suppress craving — and how that might work together with a decreased ability to monitor behavior … to make some people more vulnerable to taking drugs.”Source: online Proceedings of the National Academy of Science. May 2009

In a small pilot study, Topiramate – a medication currently used to treat seizure disorders – has helped cocaine-addicted outpatients stay off the drug continuously for 3 weeks or more. That may not seem like a long time, but previous research has shown that outpatients who avoid relapse for 3 to 4 weeks during treatment with behavioral therapy and medication have a good chance of achieving long-term cessation. In other clinical trials Topiramate has helped prevent relapse to alcohol and opiate addiction; these new results with cocaine add to hopes that it may prove a versatile treatment medication for several drugs of abuse.

Dr. Kyle M. Kampman and colleagues at the University of Pennsylvania School of Medicine and the Veteran Affairs Medical Center in Philadelphia treated 40 crack-cocaine-smoking outpatients, mostly African American males, for 13 weeks at the University of Pennsylvania Treatment Research Center (TRC). All participants met the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) criteria for cocaine dependence. They were typical of the chronic, relapsing abusers who seek treatment at the TRC: They abused cocaine an average of 10 years, preferring crack to the powder form, and demonstrated the average level of drug-related problems. However, participants’ abuse was atypical in one way; they were on the “milder end of the addiction severity spectrum measured by cocaine withdrawal symptom severity and days of abuse and money spent on cocaine,” says Dr. Kampman. On average, participants abused cocaine 6 to 8 days and spent $300 to $500 on the drug in the month before treatment compared with the 10 to 13 days and $400 to $600 reported by most patients at the facility. Because Topiramate exacerbates cocaine withdrawal symptoms, the investigators selected patients who were able to attain at least 3 days of self-reported abstinence immediately before starting the trial and who, based on their level of addiction, were not likely to enter severe withdrawal. Dr. Kampman says that about 40 percent of patients treated at the TRC experience relatively mild withdrawal symptom severity.

After a 1-week baseline period, Dr. Kampman’s team gave Topiramate to 20 study participants, and placebo to the other 20. To avoid potential Topiramate side effects, including sedation and slurred speech, they initiated treatment with 25 mg/d and increased it by 25 mg/d every week to 200 mg/d. They maintained this maximum dose during weeks 8 through 12, then tapered to zero during week 13. The patients also received cognitive behavioral coping skills therapy twice weekly throughout the study. The researchers verified cocaine abstinence two times a week with urine tests.

By the end of the 13th week, almost 60 percent of patients taking Topiramate attained 3 or more weeks of continuous abstinence from cocaine compared with 26 percent of those taking placebo. All 40 patients showed improvement from week 1 to week 13, as reflected by lower Addiction Severity Index (ASI) scores. Patients taking the medication improved more, with average scores in the topiramate group falling by 69 percent, from 0.210 to 0.066, compared with 50 percent, from 0.162 to 0.081, in the placebo group. Dr. Kampman says the improvement in ASI scores reflects fewer days of cocaine abuse and patients’ perceptions of reduced cocaine-related problems. “Patients saw the improvement in their condition, which is an important part of recovery,” he says.

“Based on our findings and other work showing this medication’s effectiveness as a treatment for alcohol and opiate addiction, topiramate appears to have great potential as a relapse prevention medication for people who have achieved initial abstinence from cocaine,” says Dr. Kampman.

Possible Mechanisms

All addictive drugs deliver pleasurable effects by enhancing the neurotransmitter dopamine in the mesocorticolimbic pathway – areas of the brain involved in reward and motivation. Topiramate seems to change the – gamma aminobutyric acid (GABA) and glutamate. Animal studies have suggested to scientists that either activating GABA-producing neurons or blocking glutamate receptors would lessen craving in cocaine-addicted human subjects. “Topiramate does both simultaneously, a unique dual action that appears to underlie its’ promise as a relapse prevention medication,” says Dr. Kampman.

“These are preliminary results, but researchers are very excited about the potential Topiramate has shown as a treatment for a range of problems, including addiction to several drugs and some impulse control disorders,” says Dr. Frank Vocci, director of NIDA’s Division of Pharmacotherapies and Medical Consequences of Drug Abuse. In addition to its initial successes in preventing relapse in patients with alcohol, opiate, and now cocaine addiction, animal studies have suggested it may attenuate nicotine addiction. “Topiramate may prove an effective treatment for patients who are addicted to multiple drugs,” Dr. Vocci adds.

Dr. Kampman plans additional studies to further evaluate Topiramate as a treatment for cocaine addiction. In addition to confirming the present results, obtained with African American male crack smokers, the medication must be tried in other racial groups, women, and powder-cocaine abusers. Dr. Kampman and his colleagues also plan to study Topiramate therapy for patients with coexisting cocaine and alcohol addiction – a group that comprises half of people treated for cocaine abuse.
• Kampman, K.M., et al. A pilot trial of topiramate for the treatment of cocaine dependence. Drug and Alcohol Dependence 75(3):233-240, 2004.

New animal research suggests that a protein called PSD-95 is linked both to cocaine addiction and learning disorders.

Over the past six years, researchers in the United Kingdom and the United States have examined molecular changes in the brains of mice. They found that the absence of PSD-95 impaired learning and memory processes. They also found that cocaine use lowers levels of the protein, which may explain the memory and coordination problems suffered by many drug users.

The researchers found that reduced levels of the protein or the complete lack of it interfered with the way the brain changes electrical activity in nerve cells into chemical activity.

“The protein molecule is important in the type of learning to do with people, places and things, so cocaine strikes at the kinds of learning which would include, for example, studying for examinations,” said Seth Grant, professor of molecular neuroscience at Edinburgh University in the United Kingdom.
The study’s findings could lead to the development of drugs that might reverse the damage and reduce drug cravings.

La Jolla, CA. June 21, 2004 — Scientists at The Scripps Research Institute have designed a potentially valuable tool for treating cocaine addiction by creating a modified “phage” virus that soaks up the drug inside the brain.They coated the virus with an antibody that binds to molecules of cocaine and helps to clear the drug from the brain, which could suppress the positive reinforcing aspects of the drug by eliminating the cocaine high.

“Typically one would think of a virus as a bad entity,” says principal investigator Kim D. Janda, Ph.D., who holds the Ely R. Callaway, Jr. Chair in Chemistry and is an investigator in The Skaggs Institute for Chemical Biology at Scripps Research. “But we are taking advantage of a property it has—the ability to get into the central nervous system.”

The structure and design of the virus and its effect in rodent models are described in an article that will be published in an upcoming issue of the Proceedings of the National Academy of Sciences.

A new study presents the highest risk for dependence on alcohol is about age 20-21 years but that for marijuana it is about 17 years. The peak for cocaine dependence was seen to occur at about age 24-26 years and was estimated to be between 18.4-24.5%. Additionally, the authors noted that 5-6% of cocaine users become dependent in the first year of use and 15- 16% had become dependent within 10 years of first use, For those who use marijuana at least once, the probably of becoming dependent was 9% by age 30 though most cases of dependence occurred when users were 15-25 years old. For those who used alcohol at least once, the “estimated cumulative probability of alcohol dependence by age 55 was about 20%… Most cases met that criteria, however, between the ages of 15 and 35 years.”

Addiction specialists have determined that people who use cocaine get sick more often because the drug hampers production of a body protein that triggers immune responses.

For the study, researchers at McLean Hospital and Harvard Medical School injected cocaine in the arm of participants who said they used the drug in the previous month. Another group was injected with a placebo. In the other arm, a catheter was placed in all participants. Generally, the presence of a foreign device, such as a catheter, increases the level of interleukin-6, a protein that tells the immune system to fend off the invader. In the group receiving the placebo injection, the protein performed normally.. But among participants receiving cocaine, the interleukin-6 level increased only one-third as much as the placebo group after four hours.Dr. John Halpern, a training doctor in a drug-detoxification unit, said the results help to explain why ‘a every single person coming in had a cold.” The study is published in the March 2003 issue of the Journal of Clinical Endocrinology and Metabolism.

New animal research shows that stimulant drugs, such as amphetamine and cocaine, could inhibit the changes that take place in the brain as a result of life experiences. Various life experiences, such as learning, physically change the brain’s structure and affect behaviour. In the latest study, researchers from the U.S. and Canada set out to examine how drug use and life experiences interact to produce changes in certain brain cells. “The ability of experiences to alter brain structure is thought to be one of the primary mechanisms by which the past can influence behaviour and cognition,” said NIDA Director Dr. Nora D.Volkow. “However, when these alterations in brain structure are produced by drugs of abuse, they may lead to the development of compulsive patterns of drug-seeking behaviours that are the hallmark of addiction.”

For the study, Dr. Bryan KoIb and his team of researchers at the University of Lethbridge in Canada and Dr. Terry Robinson and colleagues at the University of Michigan repeatedly administered amphetamine, cocaine, or saline for 20 days to individually housed rats. After 20 days, the rats were placed in a new environment for three months. Some were housed in standard laboratory cages, while others were placed in a complex environment with a variety of stimuli. At the end of three months, researchers analyzed the rats brains for changes in dendritic branching and spine density. These areas affect motivation and reward and sensory motor function. Their findings mimicked previous studies that found that amphetamine use increased dendritic branching and spine density in the nucleus accumbens and decreased spine density in the parietal cortex. However, the group of rats that had been given amphetamines and housed in the complex environment did not show the same environmental-induced structural changes in the nucleus accumbens and parietal cortex as did saline-treated animals in the complex environment. With the rats given cocaine, the researchers found that the drug blocked the environment-induced changes in the medium spiny neurons of the nucleus accumbens.

“The findings from this study indicate that at least some of the cognitive and behavioural advantages that accrue with experience may be diminished by prior exposure to psycho stimulant drugs,’ said KoIb. “This impairment of the ability of specific brain circuits to change in response to experiences may help explain some of the behavioural and cognitive deficits seen in people who are addicted to drugs.” KoIb added that additional research is needed to ‘determine whether certain experiences, such as exposure to complex or rewarding environments, can alter the ability of drugs to induce structural changes in the brain. If exposure to psycho stimulant drugs can alter the effects of subsequent experience, experience may be able to influence the later effects of drugs. It may even be possible for certain experiences to counteract the effects of psycho stimulant drugs.’The study’s findings are published in the Aug. 25 online edition of the Proceedings of the National Academy of Sciences.

Using an experimental addiction treatment first investigated at the U.S. Department of Energy’s Brookhaven National Laboratory, a team of scientists from Brookhaven, the New York University (NYU) School of Medicine, and a national addiction treatment center in Mexico report prolonged abstinence and the elimination of drug craving in eight out of 20 hard-core, long-term cocaine addicts who enrolled in the study. This is the first human clinical data showing that gamma vinyl-GABA (GVG, vigabatrin) holds promise as a pharmacological treatment for cocaine addiction.“It is extremely gratifying to see these early human results bear out what we’ve observed in our extensive preclinical animal studies with GVG,” said Brookhaven neuroanatomist Stephen Dewey, who has been using animal models and brain imaging techniques to investigate GVG’s effects on neurochemistry and addictive behavior for more than ten years. These animal experiments have shown that GVG can block drug-induced increases in brain dopamine (a chemical associated with reward and pleasure, which is elevated by all addictive drugs), drug-seeking behavior, drug self-administration and sensitization, and drug craving — even that triggered by environmental cues.

“This promising work on a potential treatment for drug addiction illustrates the value of the Department of Energy’s basic research in physics, chemistry, and imaging sciences,” said Secretary of Energy Spencer Abraham. “The advanced technologies developed in the DOE laboratories are being applied to a number of critical national health issues, including the problem of drug abuse.”Said lead author Jonathan Brodie, a psychiatrist and biochemist at NYU who also collaborated on the animal experiments, “These human clinical data support the need for a larger double-blind placebo-controlled trial that will more carefully examine the risk/benefit relationship for GVG in the treatment of cocaine addiction — a life-threatening disease for which there are currently no effective pharmacological treatments.”

The study was conducted in June and July of 2003 at a Mexican-government- designated addiction treatment center in Baja California (the Clinica Integral de Tratamiento Contra Las Adicciones in Mexicali, B.C.) at the suggestion of Emilia Figueroa, a physician familiar with Dewey’s preclinical at work on GVG. GVG is approved for use in the treatment of epilepsy in Mexico (and many other countries), but not in the United States because it can sometimes cause a reduction in the field of vision. The protocol was approved by the state of Baja California and the Mexican federal government.Twenty daily cocaine abusers who expressed an interest in breaking their drug dependence were enrolled and given an escalating daily dose of GVG, starting with one gram twice a day, and reaching two grams twice a day by day seven of the trial. The subjects were treated as outpatients, allowed to return home each day and go about their normal lives. They were encouraged to participate in group and individual therapy programs, and all were required to provide urine samples for drug screening twice weekly and complete daily questionnaires on drug use and craving.Eight subjects dropped out within the first 10 days, stating that they did not wish to stop their cocaine use. Of the 12 who continued treatment with GVG, eight achieved periods of abstinence of more than 28 consecutive days, the duration set as a benchmark for successful treatment. All eight were tapered off GVG after completion of the trial, and remained drug-free at the time of publication. Four other patients stayed in the trial for periods ranging from 25 to 43 days but continued to use cocaine, albeit in significantly reduced amounts. None of the study participants reported any visual disturbances.Those who completed the study reported that their craving for cocaine was eliminated within two to three weeks. They showed profound behavioral gains in self-esteem, family relationships, and work activities.‘The success rate achieved in this small study — 8 out of 20 remaining in the trial and drug-free –is comparable to that of other experimental cocaine addiction treatment protocols. But the prolonged duration of abstinence far exceeds what other pharmacological treatments have achieved,’ said Frank Vocci, Director, Division of Treatment Research and Development, National Institute on Drug Abuse.‘The resu!ts are particularly impressive considering that the study subjects remained in the same neighborhood, where the drug is readily available, and with all the cues and social pressures that supported their addiction for so many years,” said Figueroa.

The scientists hope that larger scale trials on GVG will be conducted at NIDA sponsored addiction research centers in the U.S. to investigate its efficacy as a treatment for addiction as well as any side effects.In October 2002, Catalyst Pharmaceutical Partners of Coral Gables, Florida, received an exclusive worldwide license from Brookhaven Science Associates, operator of Brookhaven National Laboratory, for the use of the drug vigabatrin for its application in treating drug addiction.

Results of recent research suggest that combining the antiseizure medication topiramate with one form of behavioral therapy may effectively treat cocaine addiction. Researchers with the University of Pennsylvania School of Medicine in Philadelphia enrolled 40 people in a 13- week, placebo-controlled, double-blind study. Participants received placebo or an escalating daily dose of topiramate for 8 weeks (they initially received a dose of 25 mg daily, which was increased by 25 mg per week until the maximum dose of 200 mg per day was reached during the 8th week of the study). This maximum once-daily dose was maintained through week 12. During week 13, the dose of the drug was decreased daily until participants were weaned from it.

All study participants also received twice-weekly, individual, cognitive-behavioral relapse prevention therapy. In cognitive-behavioral therapy, patients learn to confront the consequences of their drug use by recognizing the environmental cues and potentially stressful situations that trigger strong drug cravings, and develop avoidance strategies.

The scientists reported that participants who received topiramate were more likely than those who received a placebo to be cocaine-abstinent after the 8th week of the study. In addition, data from the 36 people who returned for at least one evaluation visit after starting medications showed that those who received topiramate and counseling were significantly more likely to achieve 3 or more weeks of continuous cocaine abstinence compared with those who received placebo and counseling (59 percent vs. 26 percent, respectively).

WHAT IT MEANS: A recognized treatment for seizure disorders, topiramate also has been studied for treatment of alcoholism and opiate dependence. This study, however, is one of the first to explore its usefulness as a potential treatment for cocaine addiction. This study is important because it demonstrates that topiramate can successfully produce a stable period of cocaine abstinence. Previous research indicates that achieving a stable period of continuous cocaine abstinence is a predictor of long-term abstinence.

Dr. Kyle Kampman led this NIDA-funded study.

Source: Was published online in May, 2004 in Drug and Alcohol Dependence.

Researchers at the Scripps Research Institute have developed a virus that, based on animal studies, may curb cocaine cravings in addicted individuals, the BBC reported June 22.

Researchers previously had developed proteins that reduce cocaine’s effects, but it was difficult to get them to bypass the body’s defenses. The virus, on the other hand, is able to pass the defenses in the nervous system and produce proteins where they have the most effect in curbing cocaine cravings.

Researchers injected the virus into the noses of rats twice a day for three days. On the fourth day, cocaine was administered. The scientists found that the cocaine had less effect on the animals “infected” with the virus, and showed fewer signs of behavior typical of cocaine exposure.

“We have shown a promising strategy in the continuing effort to find effective treatments for cocaine addiction,” the researchers wrote. “Whereas previous protein-based treatments have relied on peripheral drug-protein interactions, our approach delivers the therapeutic protein agent directly into the central nervous system, the site of drug action.”

Lead researcher Professor Kim Janda said the virus could be used in conjunction with abstinence programs and other vaccines.

Researchers were surprised to find how effective the drug baclofen, commonly used to treat spasticity, has been in helping individuals overcome cocaine addictions, the Medical Post reported Jan. 6.

The results of a random, double-blind study involving 70 people addicted to cocaine found that baclofen stops the release of dopamine in the brain. In doing so, the drug reduces the “high” associated with cocaine use.

The drug is particularly effective for chronic, heavy users of crack cocaine.

“I was surprised by the results of our study,” said principal investigator Steve Shoptaw, Ph.D., a psychologist at the University of California Neuropsychiatric Institute.

The study’s findings were so impressive that researchers had an independent analysis of the research done by the Biostatistics Group at Stanford University Medical Center.

In March, an eight-week clinical trial will begin in eight research centers throughout the U.S. Shoptaw said if the trial supports the study’s findings, “I think that would generate a great deal of excitement in addiction medicine.”

Source: published in the Journal of Clinical Psychiatry. Reported in Medical Post Jan 2004

Results of a study funded by the National Institute on Drug Abuse (NIDA), National Institutes of Health, suggest that disulfiram, a medication used to treat alcohol addiction, is effective in combating cocaine abuse. The researchers also conclude in the same study that combining disulfiram with behavioral therapy provides more positive results in treating cocaine dependence than disulfiram in combination with another form of therapy. The research is published in the March 2004 issue of the Archives of General Psychiatry.

In the study, 121 cocaine-dependent individuals randomly were assigned to receive disulfiram (also known as Antabuse) or a placebo, in addition to undergoing one of two behavioral therapy interventions. Participants received either cognitive behavioral therapy (CBT) or interpersonal psychotherapy (IPT) in individual sessions during the 12-week project. Results showed that participants given disulfiram reduced their cocaine use significantly compared with people given placebo. In addition, those who received disulfiram in combination with CBT reduced their cocaine use compared with those who received disulfiram in combination with IPT. Lead investigator Dr. Kathleen Carroll, of Yale University School of Medicine, and her colleagues also report that benefits seen with disulfiram and CBT were most pronounced for people who were not alcohol dependent or who abstained fully from alcohol during therapy.

“About 60 percent of people dependent on cocaine also abuse alcohol, so it was thought you could reduce cocaine abuse by targeting the accompanying codependence on alcohol,” says NIDA Director Dr. Nora D. Volkow. “But these results suggest that disulfiram exerts a direct effect on cocaine use, rather than reducing concurrent alcohol use. More research is needed about whether combining disulfiram with CBT provides an even more effective tool for treating cocaine dependence.”

Disulfiram is one of two medications approved by the Food and Drug Administration (FDA) for treating alcohol abuse. It interferes with the metabolism of alcohol, producing aversive reactions such as nausea and vomiting when alcohol is ingested. The FDA notes that aversive reactions may also occur when patients taking disulfiram use cocaine.

Cognitive behavioral therapy (CBT) theory holds that surroundings strongly influence a person’s thinking and behavior, so CB therapists teach their patients new ways of acting and thinking in response to their environments. In the case of CBT for addiction, patients are urged to avoid situations that lead to drug use and to practice drug refusal skills. Interpersonal psychotherapy (IPT) is based on the concept that many psychiatric disorders, including cocaine dependence, are related intimately to disorders in interpersonal functioning, which may be related to the origin or perpetuation of the disorders.

A decade after Colombia legalized possession of 20 grams of marijuana and one gram of cocaine and heroine for private consumption, President Alvaro Uribe wants to restore total prohibition. Legalization was aimed at forcing the government to find more effective methods than law enforcement for combating drug abuse, such as education programs. However, drug use has increased by 40% in the last 10 years and it is believed to have done so because it made drugs more acceptable in a society that traditionally frowned upon them as a source of corruption and violence.
Source:Associated Press, April 5, 2004.

The study, published in the November 17, 2004 issue of the Journal of Neuroscience, was conducted by Dr. Robert Hester of Trinity College in Dublin, Ireland, and Dr. Hugh Garavan of Trinity College and the Medical College of Wisconsin in Milwaukee. The scientists who performed the study suggest that the resulting cognitive deficits may help explain why abusers persist in using the drug or return to it after a period of abstinence.

Scientists enlisted 15 active cocaine abusers and 15 healthy individuals who have never used the drug. Each participant completed a task in which they viewed memory lists of letters for 6 seconds and “rehearsed” each list for 8 seconds. The participant then pressed a button when they were presented with a letter that was not part of the preceding “memorized” list. During the task, the participants’ brains were analyzed via functional magnetic resonance imaging (fMRI), a noninvasive imaging technique that illustrates nerve cell activity during the performance of a specific task.

Results showed that the cocaine abusers were significantly less proficient than the controls at accurately completing the task.

“Previous research that examined cognitive function in cocaine abusers identified decreased activity in the ACC,” says Dr. Garavan. “But our study is the first to show that the difficulty cocaine users have with inhibiting their actions, particularly when high levels of reasoning and decision-making are required, relate directly to this reduced capacity for controlling activity in the ACC and prefrontal regions of the brain.”
Source:The Journal of Neuroscience ; November 17, 2004

NEW YORK (Reuters Health) – A part of the brain involved in both drug craving and judgment appears to be smaller in cocaine addicts than in healthy people, researchers have found. Analyzing brain scans from 27 people addicted to cocaine and 27 healthy adults of the same age, the researchers found that in the drug abusers, a brain structure called the amygdala was smaller than normal.

Exactly what the finding means is not yet clear, but several pieces of evidence suggest that reduced volume in the amygdala may predispose a person to cocaine addiction, the study’s senior author told Reuters Health.

The amygdala is a collection of nuclei in the brain involved in the processing of emotion. Brain-imaging studies have tied drug craving to activity in the amygdala, and recent research has also suggested that the brain structure aids in sizing up the potential negative outcomes of an action.

It’s such judgment that people with drug addiction typically lack, Dr. Hans C. Breiter of Massachusetts General Hospital in Boston noted in an interview with Reuters Health.

His team’s study, published in the November 18th issue of the journal Neuron, cannot answer the question of whether smaller amygdala volume is a contributor to or consequence of cocaine addiction, Breiter said.

However, he pointed to evidence that supports a causal role. For example, amygdala volume did not correspond with the level of a person’s drug abuse; cocaine users in the study had abused the drug for anywhere from one to 27 years, yet had similar reductions in amygdala size.

In addition, Breiter explained, during normal development, the right-hemisphere amygdala becomes larger than the left. However, in these cocaine addicts, he said, “there was a loss of this asymmetry.”

It seems unlikely, the researcher noted, that drug abuse would have affected only one side of the brain in these individuals. Instead, he said, such a loss of asymmetry in the amygdala would seem to have genetic underpinnings.

But if a reduction in amygdala volume is involved in cocaine addiction, the implications would be great regardless of whether it’s a cause or effect, according to Breiter.

If even short-term cocaine abuse can cause such “dramatic” degenerative change in the brain, he said, that would highlight a prime danger of the drug.

On the other hand, if smaller amygdala volume raises a person’s vulnerability to cocaine addiction, then it offers a potential way to reveal that risk. According to Breiter, it might become possible for people with a family history of any forms of addiction to get a brain scan of the amygdala to see if they have this structural predisposition.

The fact that the amygdala appears to be involved in judging the potential pitfalls of an action may help explain how an abnormality in its structure could make a person susceptible to cocaine addiction, according to Breiter.

However, there is also the amygdala’s role in drug craving. An interesting finding, Breiter noted, was that “the smaller the amygdala was, the more they craved for cocaine.”

Whether the findings are unique to cocaine is not yet clear. The study is part of a larger project by Breiter and his colleagues that is using advanced brain imaging to find potentially inherited “markers” in the brain – such as differences in structure or nerve activity – that are associated with addiction and mood disorders such as depression.

Two related genes that help control signaling between brain cells may play an important role in cocaine addiction, says a study in the Aug. 5 issue of Neuron.

In research with mice, scientists found that deleting either of the two genes in the “Homer” family caused symptoms similar to those of cocaine withdrawal. The finding provides a new research target for trying to understand how both a genetic susceptibility to addiction and environmental factors cause addiction.

The study found the Homer1 and Homer2 genes appear to be specific for cocaine. When the researchers tested the effects of caffeine and heroin on mice that lacked the Homer genes, the rodents’ behavioral responses weren’t the same as they were with cocaine.

“While it can be anticipated that additional genetic models may be discovered that mimic or block behaviors associated with cocaine addiction, the striking concordant neurochemical phenotype between Homer2 deletion and withdrawal from chronic cocaine treatment indicates that Homer is a particularly good candidate to play a central role in cocaine addiction,” the study authors wrote.

Researchers say that the onset, pattern, and duration of the “highs” produced by cocaine and methamphetamine differ significantly — findings that could have implications for development of anti-addiction medications.

The authors from the Jane and Terry Semel Institute for Neuroscience and Human Behavior at UCLA found that cocaine-using research subjects reported a quicker peak and decline of their “high” than methamphetamine users. The body’s cardiovascular system responds quickly to both drugs, but physical responses to cocaine also decline more quickly than with meth use.

“These differences help explain patterns of use by addicts. Methamphetamine users, for instance, report using the drug daily throughout each day, while cocaine users typically engage in binges that occur most often in the evening,” said lead study author Thomas F. Newton. “In addition, the study results may impact development of medication treatments for addiction to these two very different stimulants.”

High incidence of aneurysms found in users, study finds
Cocaine users seem to have an unusually high incidence of coronary artery aneurysms, weakened areas of heart blood vessels that raise the risk of heart attacks, new research finds.

The study included 191 men and women in their 40s who had angiography, an X-ray of blood vessels, because of known or suspected heart disease. Aneurysms were found in 34 of the 112 persons who reported using cocaine and only six of 91 nonusers.

The study, by physicians at the Minneapolis Heart Institute Foundation, appears in the May 10 issue of Circulation.

That higher incidence of aneurysms may help explain why cocaine users have been found to have a high risk of heart attacks, said Dr. Timothy D. Henry, director of research at the foundation.

Henry suggested two possible explanations for the increased incidence of aneurysms.

“Cocaine use causes periodic hypertension, periods when the blood pressure goes up sharply,” he said. “Having such episodes of high blood pressure over the course of time can lead to formation of aneurysms.”

Cocaine is also known to damage the endothelium, the delicate lining of blood vessels, which could contribute to the weakening of the arteries, Henry said.

Whatever the explanation, the report is “another reason to tell people how dangerous cocaine is,” he said.

The study cited estimates by the federal Substance Abuse and Mental Health Services Administration that 27.7 million Americans – 12% of those 12 and over – had used cocaine at least once in 2001, and that 1.7 million had used it in the previous month.

Most studies of cocaine and heart damage have concentrated on immediate problems, Henry noted. The new study raises the possibility that even short-term use can cause damage decades later, he said. One man in the study who was found to have an aneurysm said he had used cocaine heavily for a two-year period 15 years earlier, Henry said, so the drug “can cause long-term damage that you have to live with the rest of your life.”

Dr. Murray Mittleman, director of the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center in Boston, said the new study “provides clues to the mechanisms of heart attacks occurring in people who are cocaine users.”

“It is an important step forward in understanding the biology of what happens in cocaine use,” Mittleman said.

But follow-up studies are needed because of the way the study was carried out, he said.

“They didn’t start out looking at people who used cocaine,” Mittleman said. “They looked at people who had angiography for some clinical reason. It is possible that this is a special group of cocaine users.”

Nevertheless, the report “gives some insight into why we observe a higher rate of cardiac problems in cocaine users,” he said.

A surge in cocaine use is pushing Britain towards a “healthcare disaster” that will see a dramatic rise in heart attacks, strokes and neurological problems among young people, says a leading specialist. The warning follows a three-year investigation into cocaine use carried out at a London hospital emergency unit which indicates that the medical complications of the drug will become a significant burden on hospital resources.

The study looked at levels of cocaine in people who arrived at the accident and emergency unit of St Mary’s hospital, Paddington, London, who were complaining of chest pains, a common side-effect of the drug. It found that on Friday or Saturday nights up to half the young people tested had cocaine in their system.

While fewer tested positive for the drug during the week, the numbers were still surprisingly high, said John Henry, a leading toxicologist and professor of accident and emergency medicine, who led the study. “Cocaine usage has peaked in the US but here it is still on the rise, which means the worst is yet to come. We’re going to see more severe addiction, more strokes and heart attacks in young people, and more of the other complications linked to its usage,” said Professor Henry, who is regarded as the UK’s leading expert on illicit drug use. “It’s a healthcare disaster and it’s coming here.”

Records taken during the study, to be published in an academic journal, show that between 7% and 10% of all those complaining of chest pains were found to have traces of cocaine in their urine. With the under-40s cocaine usage was markedly higher; a third of this group tested positive for the drug on weekdays, rising to 50% over the weekend. Tests on a control group admitted to A&E without chest pains showed only 3% had taken cocaine. The study confirms the fears of other healthcare professionals that cocaine use in Britain has reached an unprecedented level. In an audit of drug tests carried out by the City Hospital NHS teaching trust in Birmingham cocaine use was found to be increasing by about 50% every three years, a trend showing no sign of slowing. “The arrival of the cocaine epidemic has now started to become a reality in the UK,” said Stephen George, the doctor who did the survey.

The rise of cocaine has been boosted by greater acceptability of the drug and better supply, bringing more drugs to UK streets and lower prices. A gram wrap of cocaine now costs as little as £45. Experts fear cocaine use will continue to soar until it reaches a peak, as it did in the 1990s in the US where there are now 25 million users and two million addicts.

The increased availability of the drug has been picked up by coroners’ offices which have found that most heroin addicts dying of an overdose now have cocaine in their systems. “Even 10 years ago we didn’t see cocaine in those cases,” said Susan Paterson, a toxicologist at Imperial College, London, who works with coroners on more than half of the capital’s heroin deaths.

Cocaine tightens up blood vessels, making the heart work harder and raising blood pressure. While long-term heart problems can build up in cocaine users, as little as two 100mg lines (a fraction of an ounce) is enough to cause chest pains. US studies found that 5% of cocaine users attending A&E departments with chest pains had heart attacks because of their drug usage. Hospitals are already reporting patients in their early 30s suffering strokes and severe coronary heart disease brought on by cocaine use. Many do not smoke, are not overweight and do not have naturally high blood pressure.

In the US a condition called aortic dissection has become common among cocaine users. Caused by blood being forced into the lining of big vessels, it essentially creates a new channel for blood to flow down. The rupture itself causes crushing chest pains but also reduces blood flow to vital organs, leading to brain and kidney damage in many cases. A third of the cases of aortic dissection in the US are attributed to cocaine use.

The drug has also lead to a rise in foetal deaths in the US. It is believed that one in 10 babies dying in the womb do so because their mother took cocaine – a factor that leads to a rupture of the placenta, making it shear away from the womb.

Groups that deal with cocaine addicts say users are often oblivious to the harm cocaine can cause. And low prices, a poor understanding of the drug’s medical effects and wide acceptability of cocaine, mean there is little to put the brakes on its soaring popularity. “There’s no measure of an increase in heart problems yet, but I foresee it happening. We’re attacking the other risk factors for heart disease, such as smoking … but the rise in cocaine usage is the introduction of another serious risk factor. It’s already impacting on emergency services,” said Prof Henry.

The Thames is awash with cocaine as Londoners snort more than 150,000 lines of the class A drug every day.

The figure is 15 times higher than official Home Office statistics and equates to four out of every 100 people regularly taking cocaine, or up to 250,000 of the capital’s six million residents.

Londoners snort over 150,000 lines of cocaine a day

An investigation by the Sunday Telegraph found that, after cocaine had passed through users’ bodies and sewage treatment plants, an estimated 2kg – 80,000 lines – of the drug went into the river each day.

Anti-drug campaigners said last night that the findings showed that cocaine use was a ticking “health-care time bomb” and called for the Government to take drastic action.

The Thames investigation, the first of its kind in Britain, was conducted by scientists using the latest technology. It is regarded as the most accurate large-scale drug-detection method available.

Britain’s illicit cocaine trade, estimated to be worth £352.8 million a year, is thought to have caused 139 deaths in 2002, the last year of available figures – a seven-fold rise on the 1996 figure of 19.

Doctors fear that, with little routine testing for the drug in heart attack and stroke cases, the real toll may be much higher.

A U.K. detox program is using healthy snacks as a way to help addicts overcome anxiety and sleeplessness.

Crack and cocaine addicts going through detox are given snack packs that include brazil nuts and sunflower seeds — natural remedies for relaxation — along with cognitive therapy and acupuncture.

“You’ve got to want to come off crack cocaine or stimulants yourself, but the packs help like mad,” said Joe, an ex-crack cocaine user. “Once you can suppress your cravings you can get on with life. It’s working for me.”

And Karl Sheldon of the Middlesbrough, England drug-action team, added: “When it comes to drug addiction we always think of the usual stuff, opiates and physical addiction. Stimulants like cocaine and crack cocaine are more psychologically addictive, so you are looking at a different way of treating these addicts. For example, the licorice root you chew on is good for sweet cravings and also for liver function. And again with brazil nuts, the chemicals inside attach onto receptors in the brain which deal with opiates and also stimulants.

“You are not going to eat a brazil nut and all your cravings are going to go away,” continued Sheldon. “This is about dealing with your cravings and taking the edge off them.”

Sheldon said about 50 snack packs have been given to addicts over the past two months, and seem to be having a positive effect.

Cocaine use disrupts the brain’s ability to learn with new experiences, according to recent studies that looked at behavior as well as the circuitry of the brain.

UPI reported July 20 that University of Pittsburgh researchers Yukiori Goto and Anthony Grace conducted electrophysiological studies of the effect of cocaine on the prefrontal cortex and hippocampus regions of the brain, along with the nucleus accumbens, and concluded that the drug interfered with brain plasticity, or learning ability.

In corresponding behavioral studies, the researchers found that while rats sensitized to cocaine and placed in a maze were able to learn the solution to a maze with visual clues faster than other rats, they were less able than other rats to change strategies when required to ignore visual cues and always turn left or right in order to get a reward.

The researchers said that while cocaine “might not interfere with learning a response strategy, it may reduce the capacity of these animals to consider alternate response strategies. In this way, the disruption of synaptic plasticity by cocaine sensitization may contribute to the affective and context-inappropriate impulsive behaviors that are characteristic of drug addiction.”

Source: The research was published in the July 21, 2005 issue of the journal Neuron.

A DECISION by the Dutch government to decriminalise the smuggling of hard drugs could leave Britain vulnerable to a flood of cheap cocaine.

Customs officers are allowing traffickers caught at Schiphol airport, Amsterdam, with less than 3kg of cocaine to go free. The only penalty they face is the confiscation of their drugs.

In the first phase of a policy that could soon be extended to other hard drugs, the liberal measures are being applied to 35 so-called “cocaine flights” a week from the Caribbean.

Last year police caught 2,176 smugglers from the region and seized six tons of the drug. But from now on, traffickers no longer have to worry about hefty prison terms or even arrest.

The policy may prove even more controversial than Holland’s infamous “coffee shops”, where soft drugs such as cannabis have been sold openly for decades.

The Dutch authorities claim the measure will allow them to divert money spent prosecuting offenders into drug seizures. However, critics in neighbouring countries, including Britain, fear it will lead to a boom in the number of people ready to act as “mules” for drug cartels. The National Drug Prevention Alliance in Britain has warned that the policy amounts to a capitulation by the police with consequences that could spin out of control.

“This won’t just hit the UK badly. It will affect the whole of Europe,” said David Raynes, a former chief narcotics investigator for Customs and Excise. “Holland is the drugs warehouse of Europe and by not controlling its problem it’s creating an infection that will spread to all the countries around.”

In Germany the street value of cocaine has already fallen from €150 (£102) a gram to just €50 (£34), raising the prospect of a sharp rise in the number of addicts. The Dutch government has ignored a plea from Otto Schily, the German interior minister, to toughen rather than weaken its deterrent.

However, Ivo Hommes, a spokesman for the Dutch justice ministry, said the initiative could save millions spent on prosecuting and jailing offenders, allowing more funds to go into the detection and confiscation of drugs. “Locking up thousands of smugglers doesn’t solve the problem. There will always be more of them,” he said. “We’ve been honest enough to admit that we only manage to stop 15% of the drugs coming in, so we are trying something new.”

A leaked ministry memorandum, however, has suggested that the policy was adopted because the prosecution service was overburdened. It emphasised that drug-related arrests should not be permitted to “block the justice system”.

Britain’s National Criminal Intelligence Service is said to be eyeing the policy “warily”.

NEW YORK (Reuters Health) – A number of studies presented at the 36th annual meeting of the Society for Neuroscience, being held this week in Atlanta, show that cocaine use negatively affects the functioning of neurons (cells located in the brain and spinal cord), primarily in the prefrontal cortex, but also in a number of other areas in the brain.The result is a reduced ability to weigh benefits versus drawbacks, and to control behavior.

The prefrontal cortex is located in the frontal lobe of the brain. It is though to play a role in neuropsychological processes, such as orchestrating thoughts in accordance with actions, as well as other processes.

During fMRI, the subjects were asked to identify various amounts of money and rank them in order of value, or “reward.”

“More than half of the addicts could not differentiate between values,” Goldstein told Reuters Health in an interview before her presentation. The brain images showed a “disconnect,” or a “conflict pattern in response to monetary rewards,” she explained.

She noted that the prefrontal cortex is also the region in which impulse control occurs. An inability to distinguish between different values of money “means that this reward system can not be used to change behavior” in cocaine addiction.

“Although there is some improvement in function (in the prefrontal cortex) once the drug is removed, it never completely returns to normal,” Goldstein said.

Goldstein plans to study what happens in the prefrontal cortex using non-drug reward systems, and whether the value of non-drug reward systems can be amplified to change addictive behavior. She acknowledges that it remains to be determined if it is even possible to use cognitive behavioral training to increase behavioral control and decrease impulsivity in these individuals.

A record number of Britons were arrested for cocaine-related offences last year, leading some to worry about an upsurge in the drug’s popularity in the U.K.

The Guardian reported Dec. 7 that cocaine-related arrests rose 16 percent between 2003 and 2004, even as the country’s justice system dealt with fewer heroin and ecstasy related offences. Overall, Class A drug-related offences rose 2 percent in the U.K. last year, Britain’s Home Office reported.

A government spokesperson attributed the rise in cocaine cases to better law enforcement. “The government’s strategy is to focus on the drugs which cause the most harm and deal robustly with those who supply them,” a Home Office spokesperson said. The U.K. has recently downgraded law-enforcement efforts targeting marijuana in order to devote more resources to harder drugs.

Source: The Guardian newspaper 7th Dec. 2005The NDPA would draw attention to the research which shows that heavy use of marijuana leads to a statistically significant increase in the use of cocaine. Lax marijuana laws lead to more use of marijuana – it is not surprising therefore that there will be an equivalent increase in the use of cocaine.

Young African Americans who use cocaine are six times more likely to suffer a potentially lethal episode of bleeding inside the brain than non-users, a case-control study of major risk factors for intracerebral haemorrhage in this population conducted by researchers at the University of Buffalo and Emory University has found. The study, published in the July issue of Ethnicity and Disease, also shows twice the incidence of hypertension and five times the number of people with hypertension who weren’t taking their blood-pressure medicine among those who had had an intracerebral haemorrhage, compared to healthy, age-matched controls. Alcohol use also was associated with an increase in risk.

“African-American patients experience a two-fold higher risk of intracerebral hemorrhage compared to white patients,” said Adnan I. Qureshi, UB assistant professor of neurosurgery and lead author on the study. “This high incidence of intracerebral haemorrhage contributes significantly to death, disability and loss of productivity in young populations.

“In the absence of any definitive treatment for intracerebral haemorrhage, significant stress needs to be placed on primary prevention and understanding of factors that predispose to a higher risk in young African Americans,” he said.

Internal bleeding, also known as intracerebral haemorrhage (ICH), can occur in any part of the brain. Blood may accumulate in the tissues as well as in the space between the brain and the membranes covering the brain, a subarachnoid haemorrhage. Bleeding may be isolated in a part of one cerebral hemisphere (lobar intracerebral haemorrhage) or occur in other brain structures, such as the thalamus, basal ganglia, pons, or cerebellum (deep intracerebral haemorrhage).

ICH occurs in about 20 out of 100 000 people, statistics show, and can affect any person regardless of age, sex or race, but appears to occur more frequently in African Americans, striking the young and middle-aged disproportionately. The incidence of intracerebral haemorrhage in African Americans reaches nearly 50 out of 100 000 persons, Qureshi noted.

Since there is no effective treatment for ICH, prevention takes center stage, but little information has been available on the factors that put this population at higher risk. This study is the first to use a case-control approach to tease out these risks. It assessed health and lifestyle histories of 122 African Americans between the ages of 18 and 45 admitted to a public hospital in Atlanta with ICH between December 31, 1997, and January 1, 1990. This information was compared with data from 366 African Americans in the same age group without the condition who took part in the most recent National Health and Nutrition Examination Survey (NHANES Ill).

Researchers included data on hypertension, diabetes, smoking, cocaine use, alcohol use, and stroke or heart disease from all participants, as well as the record of prescriptions for hypertension medication and compliance with their use.

Results showed that cocaine use was the strongest risk factor associated with ICH in this population, even higher than hypertension, Qureshi said. “While the mechanism for this association isn’t clear, we suspect that the sudden elevation in blood pressure that occurs immediately after using cocaine may cause an existing aneurysm or artenovenous malformation (AVM) in the brain to rupture.” Several clinical studies of stroke among cocaine users have found a high frequency of aneurysm or AVM, he noted.

Hypertension, particularly in those who had been prescribed medication but took it irregularly, also was shown to be an important high-risk factor for ICH. These findings suggest that physicians should focus more on compliance than on screening, Qureshi said.

“In chronic hypertension, the body develops a certain protective response in an effort to counter high blood pressure’s effects. Taking blood-pressure medication intermittently may impair the development of this response and may make patients more vulnerable to blood pressure fluctuations.”

The bottom line, Qureshi said, is that a reduction in the high rate of death and disability associated with intracerebral haemorrhage can’t occur without effective preventive measures.

“The study demonstrated the presence of factors in the community that easily can be modified to reduce this risk. These include avoidance of cocaine use and regular use of blood pressure medication as prescribed.”

A drug that Duke University Medical Center researchers have successfully used to help some people quit smoking may also help curb cocaine cravings, according to studies conducted in rats.

The drug mecamylamine, used in combination with nicotine to help reduce the urge to smoke cigarettes, has now been shown in animal studies to reduce their self-administration of cocaine. Rats that were trained to press a lever in order to get cocaine no longer pressed it with the same frequency after they were given mecamylamine, said Edward Levin, lead author of the study. When injected with mecamylamine, the mice infused cocaine 11 times per hour, versus 19 times per hour when they received a placebo injection of saline – a reduction of more than 40 percent. “It’s always very exciting when a drug used for one addiction has implications for a broader range of addictive drugs,” said Levin, whose study was funded by the National Institutes of Health. Mecamylamine is an older medication originally used to treat high blood pressure. Researchers now know it blocks some of nicotine’s ability, and potentially that of other drugs, to generate feelings of pleasure in the brain. Levin said it works by occupying specific sites, called “nicotinic receptors,” on nerve cells where nicotine would normally act. When mecamylamine blocks these receptors, nicotine can no longer exert its full action, that of stimulating the release of dopamine. Dopamine is the primary brain chemical involved in generating pleasure. Drugs like nicotine, alcohol and cocaine all increase available amounts of dopamine and thereby increase the pleasure sensation, said Jed Rose, chief of the Nicotine Research Program at Duke and study co-author. Eventually, the brain may prefer the drug over natural rewards like food or sex, and hence, the person can become addicted. Mecamylamine blocks the action of nicotine, and potentially cocaine, by lowering the net amount of dopamine available in the brain. While cocaine still boosts available levels of dopamine, its overall amount is decreased because mecamylamine has plugged up some of the nicotinic receptor sites where the brain would naturally be activating its own dopamine. “In other words, the brain has its own chemical, acetylcholine, that stimulates the release of dopamine. Mecamylamine comes along and occupies some of the nicotinic acetylcholine receptor sites and prevents them from activating dopamine,” Rose said. “So the net effect is that less dopamine is being produced, even when cocaine comes along and boosts dopamine levels through a different pathway.” Rose said the person still desires nicotine or cocaine, but the desire is weakened because the brain is no longer being flooded with dopamine. “Mecamylamine reduces desire, but it doesn’t quench it,” he said. “Yet given how few medications there are to combat serious addictions, even a medication that reduces craving can be of significant benefit.” Already, mecamylamine has proven to be of significant benefit in helping people quit smoking.

In earlier Duke studies, Rose demonstrated that using a patch with nicotine and mecamylamine together helped 40 percent of smokers quit for at feast one year, while only 15 percent of smokers were able to do so using the patch alone. The researchers expect mecamylamine to be approved for smoking cessation sometime this year.

The trauma that a majority of drug addicts suffer in early life has now been shown to increase their vulnerability to drug addiction, Yale researchers report in a new study. “Using well-established animal models, we’ve found strong evidence that early life stress enhances vulnerability to drug addiction,” said Therese A. Kosten, assistant professor of psychiatry at Yale School of Medicine. “This study demonstrates the need to target drug abuse prevention strategies to children with early life traumas.”Rat pups that were separated from their mothers for one hour per day during the first week of life learned to self-administer cocaine more readily when they were adults compared to rats that had not had this early life stress. This effect was not due to differences in learning or general activity levels. “Previous studies show that most drug addicts have had early life trauma,” said Kosten, principal investigator on the study. “Given that 1.8 million Americans are currently using cocaine, this information will be valuable in directing future research toward potential interventions for children with early stress experiences in order to reduce the risk of developing drug addiction in adults.”Kosten and her team tested 14 adult rats, eight of which had experienced the stress of isolation from their mother, siblings and nest three months earlier. Compared to six rats that had not experienced this stress, isolated rats learned to press a lever to receive a cocaine infusion in two-thirds the number of days, and at half the dose needed for the non-isolated rats. Kosten said the groups did not differ in the number of days to learn to press a lever to receive food pellets, demonstrating that the isolation effect was specific to cocaine.

Researchers at The Scripps Research Institute have developed a second-generation, long-lived cocaine immunoconjugate that blocks cocaine passage into the brain of rats.The new immunoconjugate displays two amide groups in the stereochemical configuration found in the cocaine framework, so that antibody affinity to cocaine is optimized, Dr. Janda and associates report in the Proceedings of the National Academy of Sciences.Rats were immunized with the vaccine and challenged with systemic cocaine. Compared with unimmunized controls, locomotor activity was significantly reduced, as were stereotypic patterns of behavior, such as sniffing and rearing. Effects were sustained throughout the 12 days of the study.“We have been able to tap into the immune system to immobilize antibodies to recognize cocaine as foreign and remove it from the body,” Dr. Janda said. “The current vaccine provides a much longer lasting effect than our previous vaccines, suggesting that boosting requirements would be minimal and the antibody circulation time would be increased.”Dr. Janda added that the vaccine would be of most use in addicts who are motivated to stop using cocaine. “Typically an addict will relapse several times before he or she will ‘kick’ the drug,” he said. “We believe the vaccine will protect addicts at weak moments when they have the urge to get high. If we can prevent the high we can prevent relapse and this would speed the process of kicking the addiction.”

Medical examiners taking part in the Drug Abuse Warning Network (DAWN) said that overdoses of heroin, cocaine, and alcohol mixed with other drugs topped the causes of drug-related deaths in 2000, Substance Abuse Funding News reported April 9.The report, ‘Mortality Data from the Drug Abuse Warning Network 2000’, found that in 30 cities, more than half of the deaths reported to DAWN were drug-induced and involved multiple drugs. The data was based on death reports made to DAWN in 2000 from 137 medical examiner jurisdictions from 43 cities.Among the jurisdictions taking part in the study, the highest number of drug-related deaths were reported from Los Angeles, Calif, 1, 192; Philadelphia, Pa., 942; New York City, N.Y., 924; Chicago, Ill., 869; and Detroit, Mich., 704.Source: The Substance Abuse and Mental Health Services Administration (SAMHSA). May 2002

A study on patients visiting the emergency department at a British hospital found a growing number of people complaining of chest pains after taking cocaine. For the research, professor John Henry of Imperial College London anonymously tested the urine of 450 men under the age of 30 who visited the emergency department at St. Mary’s Hospital complaining of chest pains.

Henry, one of the country’s leading drugs experts, found that one in three of the men tested had used cocaine. According to Henry, the majority of cocaine users are unaware of the serious health risks linked to using cocaine. Cocaine use puts massive pressure on the heart, which is why doctors are seeing more young people whose hearts resemble people twice their age.

“The public image it has is of being something recreational and mild, which is very far from the truth,” said Henry.Cocaine use in Britain has increased in recent years because of a drop in its price. According to findings from the British Crime Survey, cocaine use rose by 30 percent in one year. In addition, deaths associated with cocaine increased to 95 last year from 18 in 1996.The study’s findings are expected to be published in the British Medical Journal later this year.

People who drink, smoke and take drugs could be more at the mercy of their genes than was previously realised, research showed . A study involving more than 20000 people has suggested that particular genes can influence personality traits linked to unhealthy behaviour.

Cancer Research UK scientists at Oxford University pooled data from 46 separate studies looking at the link between human behaviour and inheritance. The research focused on genes that control chemicals used to transmit signals between brain cells. Researchers found that one version of the human serotonin transporter gene (5HTT-LPR) was strongly associated with anxious personalities. Individuals with this gene variant were the sort who find social interaction stressful and may take refuge in substance abuse. The scientists found a weaker link between a variant in a second gene, the dopamine D4 receptor, and extrovert personality traits. Such people are more likely to smoke or take drugs because of a tendency to gamble with their health and seek out novelty.

The chief researcher, Dr Marcus Munafo, said: “Our study suggests that there is a genetic basis to certain kinds of personality trait, which may be important in influencing whether people take up habits like smoking or whether they can subsequently give them up. Understanding genetic influences on personality is important if we are to design health campaigns that are effective for the widest possible range of people. “We also know, through drugs such as antidepressants, that is possible to influence these behaviours, and our research may open the way to new types of medication to help people overcome cancer-causing addictions.”

Scientists do not know precisely why particular genetic variants may influence personality, but have some clues. The 5HTT-LPR variant appears to reduce levels of the serotonin transporter molecule, in turn influencing levels of serotonin activity. Serotonin helps to control emotions such as anxiety and depression. Variations in the dopamine D4 receptor seem to alter the brains response to dopamine, which is thought to be associated with novelty seeking behaviour and pleasure, and may have a role in substance abuse.
Source: Journal of Molecular Psychiatry June 2003

Thousands of cocaine-abusers are putting hospital casualty wards under strain by turning up with serious chest pains caused by taking the drug, according to a study by one of Britain’s leading authorities on drug abuse. Hospital staff have to drop other cases to deal with the drug-takers – all young men under 30 – as potential medical emergencies because the symptoms are so serious.

The research, by John Henry, a professor of medicine at Imperial College London School of Medicine, found that one in three such visits to occident and emergency departments in inner-city hospitals may be due to cocaine abuse. Prof Henry conducted anonymous urine tests on 450 men who came to his A&E department with chest pains over several months and found that a third tested positive for cocaine. The study, provides worrying evidence that the surge in cocaine use will result in a tide of heart disease in young people. Prof Henry, a former director of the National Poisons Unit who is based at St Mary’s Hospital, London, said: ‘This is a lower rate than some American studies have found, but higher than we expected, and very worrying.’ He said that the number of deaths from cocaine had been seriously underestimated. Government figures show that the number of cocaine-related deaths reported by coroners offices rose by 42 per cent last year, to 95. Prof Henry believes that the official figures are “the tip of the iceberg” because many go unrecorded as cocaine-related deaths. “They do not include all the trauma; people shooting other people or when someone gets a knife in the chest,” he said.

Casualty departments in other inner-city hospitals are experiencing a similar rise in numbers of men complaining of chest pains that are probably cocaine-related. Mr Manolis Gavalas, an A&E consultant at University College Hospital, said; ‘We frequently get people coming in with cocaine-induced chest pains. The drug is constricting the coronary circulation, so of course its dangerous – and it can lead to heart attacks. “Ten years ago it was unheard of, but now we see lots of young male patients in their 20s or 30s with this, especially on Friday and Saturday night,” he said. “If you see one of these young patients with these symptoms you know its cocaine, but its still very serious and you have to take it very seriously.’ That means the patients are given priority treatment, have medical histories taken and often have electrocardiogram readings.

Dr Carole & Gavin, a consultant at the Hope Hospital in Salford, Manchester, said: “We do seem to see more young men with these symptoms. There have been a couple in the last six months who’ve had serious chest pains and who’ve admitted using cocaine. But of course there may be many who don’t admit they’ve been using it.”

Cocaine induces a feeling of well-being by raising dopamine levels in the brain, but also increases blood pressure and causes blood vessels to contract. Sometimes the arteries feeding the heart go into spasm, causing the severe chest pains which make users go to hospital. If the spasms are particularly severe the patients may need drugs such as nitrates to force their vessels open and prevent a heart attack. Four years ago the Journal of the American Medical Association reported that the risk of death from a heart attack rose 24-fold in the first hour after cocaine use. “There’s also the risk of cerebral haemorrhage and stroke” Dr Gavin added. We’ve seen one 40-year-old in the last year who had a stroke on cocaine.”

Some researchers even fear that cocaine, along with ecstasy, could spark the early onset of Parkinson’s disease, by causing the body to exhaust its supply of dopamine prematurely. Prof Henry was so concerned about the more immediate ill-effects of cocaine that he persuaded his medical ethics committee to allow him to test urine samples from young men appearing in his hospital with chest pain in such a way that they were anonymous and could not be traced. He hopes to do follow-up research on the cost implications for the NHS.
The study comes as the Home Office prepares to publish research suggesting that the number of cocaine users in Britain has been radically underestimated. Current figures show that the number of users has risen fivefold in the past 10 years, from one in 100 to one in 20 of the 16 to 59 age group. Research it commissioned from National Economic research Associates warns, however, that many users go unnoticed. Edward Bramley-Harker, who led the research, said: “The current estimate came from looking at people arrested for cocaine abuse. But there are many affluent users who are not likely to be arrested, so the figure of 475,000 users is a considerable underestimate.’
Neither do these figures include the growing, 200,000-strong group of crack cocaine users who are at risk from the same physical side effects as users of ordinary cocaine.
Source: Daily telegraph Oct 2003

Crack cocaine has replaced ecstasy and heroin as the drug of choice among many young adults in the United Kingdom. In particular the use of crack cocaine has increased among ravers and prostitutes, the Observer reported Dec. 29.“Tackling Crack’ a new report from Britain’s Home Office, shows that the use of crack cocaine has grown more than 200 percent over the past three years. The biggest increase has been within the sex industry.In addition, DrugScope, an anti-drug group, reports that many club goers have switched to crack over fears of the effects of ecstasy use.“There is growing evidence that clubbers are under the mistaken belief that cocaine is a safer option,” said a spokesman for the charity. “Because they haven’t seen scare stories about cocaine or crack, they believe that it is a better option than ecstasy.”In Scotland, police said that crack cocaine is the drug of choice for middle class club-going teenagers. According to Tom Wood, deputy chief constable of Lothian and Borders Police, there has been a 200% increase in the use of the drug.Crack cocaine is an emerging threat,” said Wood. He added that dealers sell young people smaller ‘clubbing rocks.’U.K. drug officials said the spread of crack cocaine is a result of Jamaican dealers who have introduced the drug in London and other major cities.

Addiction researchers who met this summer to study treatment methods are close to crafting a new approach to preventing relapse,“The goal is to crack the addiction code — and the code lies in the basic working of the brain,” said Dr. George Augustine, a researcher at Duke University Medical Center. “We don’t know how addiction happens. It’s been a complete black box until recently. Now, there’s a crack of light.”Researchers said treatment success lies in a targeted approach. For instance, cocaine addiction could be treated with customized psychotropic drugs targeting specific areas of the brain. “Our objective is to revolutionize drug development and provide a completely new view of psychiatry,” said Dr. Hans Breiter, a psychiatrist and researcher at Massachusetts General Hospital in Boston.Breiter, an expert on brain imaging, and his research partner, Dr. Greg Gasic, recently received a $7.9 million federal grant for an imaging and DNA study. The clinical trial will include a total of 900 cocaine-addicted individuals, depressed individuals, and a control group of people neither addicted nor depressed. The purpose of the study is to identify brain patterns that may reveal individuals who are susceptible to addiction. Researchers want to link genetic similarities and brain circuitry to depression and drug use to create an individualized approach to treatment.“The issue is not to develop medication that changes the genes,” said Breiter, “but to move addicts back to a place where their genes are in balance.”Additional researchers also are examining the links between psychiatric disease and addiction. “People with psychiatric disorders have a much higher propensity to use drugs,” said Dr. Bertha Madras, a professor and researcher who works with non-human primates at Harvard Medical School. “Between 55 percent and 75 percent of cocaine users have psychiatric problems at birth.” Since addictive drugs cause molecular changes in the reward circuitry of the brain, researchers also want to pinpoint which molecules have been altered by drug use and find ways to reverse the effects.“A major cause of relapse is the long-lasting adaptations that have occurred in the brain in response to drugs of abuse,” said Stanford University psychiatrist Dr. Robert Malenka. “What commonly happens is that someone who has a problem with addiction is abstinent, but will be exposed to some environment where they used the drug or some person they’ve used the substance with. Then, they get these overwhelming memories we call cravings that become so powerful they have to start using drugs again.”

LONDON: British deaths from ecstasy, cocaine and amphetamines have rocketed 47 per cent in the past year.The toll topped 1500 for the first time, fuelled by a rise in so-called “recreational hard drugs taken by weekend users.Ecstasy, cocaine and speed are increasingly used by young people who take cocktails of drugs every weekend.The findings emerged in a study of coroners reports which suggested stronger tablets, easier availability, falling prices and the growing popularity of drug cocktails were behind the rising death toll.Dr Fabrizio Schifano, who led the research at the European Centre for Addiction Studies at St George’s Hospital Medical School in South London, said recreational users did not see themselves as addicts or considered they were at risk of dying’ Schifana said.Many weekend users took a cocktail of drugs and alcohol in sessions of up to 12 hours.In dozens of fatal cases, the victims also smoked cannabis.Cocaine was involved in 147 deaths lost year, a 47 per cent rise on 2001, Amphetamines were linked to 53 deaths, a 60 per cent rise. There were 64 ecstasy-related deaths, up 34 per cent.Dr Schifono so that even a small amount of a drug could kill a hardened user who had built up a tolerance over months or years. In a process called “reverse tolerance”, the user suddenly become acutely sensitive and died.The first death in Britain from a new synthetic form of morphine called Oxycontin was recorded ast year.Called “hillbilly heroin” it has killed hundreds in the US.Overal drug-related deaths rose by about 6 per cent on 2001 last year – from 1495 to 1583, About 45 per cent were due to heroin, morphine and other drugs.The greatest increase in drug-related deaths were in West London. Brcdgend and Glamorgan Volleys, West Yorkshire, Nottinghamshire, North Northumberland and East Lancashire.

Two related genes that help control signalling between brain cells may play an important role in cocaine addiction, says a study in the Aug. 5 issue of Neuron.

In research with mice, scientists found that deleting either of the two genes in the “Homer” family caused symptoms similar to those of cocaine withdrawal. The finding provides a new research target for trying to understand how both a genetic susceptibility to addiction and environmental factors cause addiction.

The study found the Homer1 and Homer2 genes appear to be specific for cocaine. When the researchers tested the effects of caffeine and heroin on mice that lacked the Homer genes, the rodents’ behavioral responses weren’t the same as they were with cocaine.

“While it can be anticipated that additional genetic models may be discovered that mimic or block behaviors associated with cocaine addiction, the striking concordant neurochemical phenotype between Homer2 deletion and withdrawal from chronic cocaine treatment indicates that Homer is a particularly good candidate to play a central role in cocaine addiction,” the study authors wrote.

In the UK, the social and economic costs of drug misuse account for between £10 billion and £18 billion a year. Around 250000 problematic drug users’ contribute to 99% of these costs.1 These addicts spend around £16,500 a year each to feed their habits, with most of this coming from the proceeds of crime2. Hard drug users, who indulge in heroin, crack cocaine and powder cocaine, are responsible for 50% of all crimes3.

On the one side, them are proponents of ‘harm reduction’. In the case of heroin, they want to see persistent users prescribed heroin under the NHS.

Opponents compare the Dutch and Swedish approach to drugs over the last 25 years, and point out that drug use in the Netherlands, which has adopted a policy of ‘harm reduction, has seen use of cannabis amongst the young more than double, with use of ecstasy and cocaine by l5 year olds rising significantly.

By contrast, in Sweden, the goal has been to create a ‘drugs free society,’ with everyone from the police to schools working towards such a strategy. As a result, overall lifetime prevalence of drug abuse, amongst 15-16 year-olds. is 8% in Sweden, compared to 29% in the Netherlands. In 1998, only 496kg of cannabis were seized in Sweden, compared to 118 in the Netherlands, now described as the drugs capital of Western Europe5 . This is because in Sweden drug use is seen as inimical to a civilised, tolerant society, whereas in the Netherlands drugs have been accepted as a ‘way of life’ and have contributed hugely to crime.

The UK’s approach to drugs is deeply flawed. with the government sending out confusing and misleading messages. Cannabis has been downgraded from a class B to class C drug; yet many people widely believe that cannabis has been decriminalised.

The ‘Lambeth Experiment’, which led the way to reclassification, caused an explosion in the number of drug dealers preying upon the area6. The experiment has to all intents and purposes ‘allowed’ people to smoke cannabis publicly. But, the moral and ethical question still remains: is it acceptable to tolerate something which is proven to damage both the health and judgement of individuals, and can also affect relationships with families, friends and the wider society?

There are now several experiments being conducted across Europe in an effort to contain heroin addiction. In Switzerland, since 1994, 1,000 of the country’s 33 heroin addicts have been prescribed pure heroin. The aim is to stabilise the health of addicts and prevent them from using heroin in public, thus taking their habit away from the black market.

Swiss officials claim that the experiment is working because crime is down, However, addicts are now becoming dependent on prescription heroin and hopes of weaning them off the substance have quickly faded.

The Police Federation disputes that legalisation would cut crime. This assumes that the powerful international drug cartels would simply fade away into the night. More likely scenarios are that they would fight to maintain their lucrative street trading.

Notes
1. The Government Reply to the Third Report from the Home Affairs Committee Session 2001-02: The Government Drug Policy: Is it working?, p.5
2. Home Affairs Third Report: The Government Drug Policy. Is it working?, Illegal Drugs, Drugs-related property crime. no.36 3.The Government Reply to the Third Report from the Home Affairs Committee session 2001-02: The Government Drug Policy. Is it working?, p.5
4 .Home Affairs Select Committee Report: The Government Drug Policy. Is it Working? Memoranda of Evidence – no.16 (submitted by the Criminal Justice Association)
5. Risk of Legalising Cannabis Underestimated: A Comparison of Dutch and Swedish Drug Policy. Criminal Justice Association, February 2002
6. The Dealers Think They’re Untouchable Now’, The Observer, 24 February 2002 and ‘London’s Drug Crime Hotspots Revealed. Evening Standard. 28 May 2003
7. Better Ways’. The Economist, 26 July 2001
8. Quoted in Home Affairs Select Committee Third Report: The Government ‘s Drugs Policy. Is Working’., no.60

Marijuana indicators continued upward trends that began in the early 1990s. In 2002, however, marijuana ED mentions stabilized, after rising from almost 600 to 1,200 from 1999 to 2001. When found as the sole drug in a hospital ED situation, patients typically present with symptoms of a panic or anxiety attack.

As in past years, marijuana precipitated more admissions into addiction treatment programs than any other illicit drug in the Twin Cities in 2003. Overall, one out of five (22.8 percent) people entering addiction treatment programs reported marijuana as the primary substance problem, compared with only 8 percent in 1991. Most (77.3 percent) were males, and 68.3 percent were white. For many, it was the first treatment experience (44.2 percent), which can reflect a relatively short abuse history. The average age of first marijuana use was 13.7 years.

Marijuana was overwhelmingly the primary drug among adolescents and young adults in treatment. Among treatment admissions under age 18, a whopping 73.2 percent reported marijuana as the primary substance problem, and among youth age 18 – 25, 34.8 percent. In contrast, among patients age 26 to 34, 14.6 percent reported marijuana as the primary substance problem, and among patients 35 and older, only 4.5 percent.

In 2003 in Minneapolis, 48.3 percent of adult male arrestees tested positive for marijuana. Nationwide, it ranged from a high of 54.9 percent in Oklahoma City, to a low of 30.9 percent in Honolulu and 31.9 percent in Salt Lake City. The median across all cities was 44.1 percent.

Marijuana, readily available according to multiple sources, sold for $5 per joint, and could be purchased by any metropolitan area middle school student. Standard, commercial grade marijuana sold for $50 per quarter ounce, $150–$175 per ounce, and $600–$900 per pound. Higher potency “BC Bud” from British Columbia was increasingly available and sold for $100 per quarter ounce and up to $600 per ounce.

Marijuana joints that are dipped in formaldehyde, which is often mixed with phencyclidine (PCP), are known as “wets,” “wet sticks,” “water,” or “wet daddies.” Marijuana joints containing crack cocaine are known as “primos.”

Harm reduction advocates claim that needle exchange programs reduce HIV risk by allowing injection drug users to continue to abuse drugs with clean needles, rather than sharing needles that may be infected with HIV. A new study finds that drug abuse may actually increase HIV infection risk by compromising the immune system, and thereby making it easier for HIV and other infectious disease to take hold. This new data potentially explains why drug abusers have higher rates of infection than other at risk groups and why areas with long-standing and high volume needle exchanges– such as Vancouver, British Columbia and Baltimore, Maryland– have failed to curtail the spread of HIV and hepatitis among the injection drug using population. Prevention and treatment for drug abuse, therefore, remain the only proven and scientifically sound prevention strategies against HIV and the other health risks associated with drug abuse. Needle exchange merely allows addicts to continue the very behavior that comprises their immune system and makes them more susceptible to HIV infection.

Cocaine abusers are more likely than nonusers to suffer from HIV, hepatitis, sexually transmitted diseases, and other infections. Most of this increased incidence is the result of conditions and behaviors–for example, injecting drugs, poor nutrition, and unsafe sex–that are often are associated with drug abuse. Now, NIDA-supported investigators at the McLean Hospital Alcohol and Drug Abuse Research Center in Belmont, Massachusetts, have found that cocaine itself has a direct biological effect that may decrease an abuser’s ability to fight off infections.

Dr. John H. Halpern, along with colleagues at McLean Hospital and Harvard Medical School, found that a key immune system component, a protein called interleukin-6 (IL-6), responded less robustly to an immunological challenge in male and female abusers injected with cocaine than in those who received placebo. “When your body detects a foreign object, IL-6 helps trigger the release of a cascade of other immune system components that isolate and neutralize the threat,” explains Dr. Halpern. “If the balance of this response is

disrupted, your body cannot fight infection as effectively as it should.”
The study involved 30 participants (16 women, 14 men, ages 21-35) with a history of cocaine abuse, including at least one drug administration within the past month. The investigators placed an intravenous catheter in one arm of each participant and measured IL-6 levels. The catheter is detected as foreign by the body’s immune system and triggers an immune response. After 30 minutes, the researchers injected cocaine or saline solution (0.4 mg/kg) into each participant’s other arm; 4 hours later, they measured IL-6 levels again. In participants given saline, IL-6 levels had more than quintupled in response to the presence of the catheter, increasing from an average of less than 2 trillionths of a gram (picograms, or pg) per milliliter of blood to an average of more than 11 pg/ml. In men and women who received cocaine, however, IL-6 levels barely doubled–from less than 2 pg/ml to an average of 3.8 pg/ml.

“The findings in this study show that in people with a history of cocaine abuse, exposure to the drug establishes conditions that can lead to immediate harm,” Dr. Halpern says. “In such subjects, we found that cocaine impairs the body’s defense system for at least 4 hours. We can’t rule out the possibility that IL-6 response returns to normal shortly after that time. But even if the blunted immune response lasts only a few hours, it makes it more likely that an infection like HIV or just a common cold can take hold,” Dr. Halpern says.

“This research suggests a link between cocaine use and compromised immune response and could help explain the high incidence of infectious disease among drug abusers,” observes Dr. Steven Grant of NIDA’s Division of Treatment Research and Development. “It reminds us that the health consequences of drug abuse reach far beyond disruption of the brain systems involved in abuse and addiction.”

The findings also have significance in another context, Dr. Grant adds. “The IL-6 findings are a small but possibly significant part of a much larger study designed to gather a wide range of information on the acute and chronic effects of abused drugs on the brain, endocrine system, and immune function. This kind of discovery-based research can yield unexpected, sometimes important, insights.”

The number of admissions to substance abuse treatment for adolescents ages 12 to 17 increased again in 2002, continuing a ten-year trend. These data were released today in the “Treatment Episode Data Set: National Admissions to Substance Abuse Treatment Services 1992-2002” by the Substance Abuse and Mental Health Services Administration (SAMHSA).

The new data show that the number of adolescents ages 12 to 17 admitted to substance abuse treatment increased 65 percent between 1992 and 2002. In 1992, adolescents represented 6 percent of all treatment admissions. By 2002, this proportion had grown to 9 percent. This report expands upon data published in May in the “Treatment Episode Data Set (TEDS) Highlights 2002.”

The increase in substance abuse treatment admissions among 12 to 17 year olds was largely due to the increase in the number of admissions in this age group that reported marijuana as their primary drug of abuse. Between 1992 and 2002, the number of adolescent treatment admissions for primary marijuana abuse increased 350 percent. In 1992, 23 percent of all adolescent admissions were for primary marijuana abuse. By 2002, 63 percent of adolescent admissions reported marijuana as their primary drug.

“The youthfulness of people admitted for marijuana use shows that we need to work harder to get the message out that marijuana is a dangerous, addictive substance, SAMHSA Administrator Charles Curie said. All Americans must begin to confront drug use and drug users honestly and directly. We must discourage our youngsters from using drugs and provide those in need an opportunity for recovery by encouraging them to enter and remain in drug treatment.”

Forty-eight percent of all adolescent treatment admissions in 2002 involved the use of both alcohol and marijuana. Admissions involving these two substances increased by 86 percent between 1992 and 2002.

In 2002, more than half (53 percent) of adolescent admissions were referred to treatment through the criminal justice system. Seventeen percent were self- or individual referrals, and 11 percent were referred through schools.

The TEDS report provides detailed data on admissions to substance abuse treatment for all age groups. The 2002 data show that polydrug abuse (abuse of more than one substance) was more common among TEDS admissions than was the abuse of a single substance. Polydrug abuse was reported by 55 percent of all admissions for substance abuse treatment in 2002. Alcohol, marijuana and cocaine were the most commonly reported secondary substances. For marijuana and cocaine, more admissions reported these as secondary substances than as primary substances.

This new report provides information on the demographic and substance abuse characteristics of the 1.9 million annual admissions to treatment for abuse of alcohol and drugs in facilities that report to individual state administrative data systems. The report also includes data by state and state rates.

Today, the Florida Department of Law Enforcement (FDLE) released the Florida Medical Examiners Commission’s Report on Drugs Identified in Deceased Persons. The report contains information compiled from autopsies performed by medical examiners across the state in 2003. During that period there were approximately 170,000 deaths. According to the report, 6,767 individuals examined had drugs in the system.

The report reveals a decrease in the incidences of Heroin in 2003 when compared with 2002. This decrease includes cases in which the drug levels found during the exams were both lethal and non-lethal. In addition, the report indicates the three most frequently occurring drugs found in decedents were Ethyl Alcohol (3,467), all Benzodiazepines (1,794), and Cocaine (1,614). The drugs that caused the most deaths were Cocaine, all Benzodiazepines, Methadone, Oxycodone, Ethyl Alcohol, Heroin, Alprazolam, and Morphine.

The three drugs that were the most lethal, meaning more than 50 percent of the deaths were caused by the drug when the drug was found, were Heroin (88 percent), Fentanyl (63 percent), and Methadone (60 percent). The report also reveals that excluding newly tracked prescription drugs, prescription drugs of Benzodiazepines, Hydrocodone, Methadone, and Oxycodone continued to be found more often than illicit drugs in both lethal (60 percent) and non-lethal (55 percent) levels during 2003.

“This report shows that with few exceptions, both illicit and prescription drugs persist in being a continuing and increasing danger to the citizens of the State of Florida,” said FDLE Commissioner Guy Tunnell. “While heroin deaths have decreased over the past year, most of the other illicit and prescription drug deaths remain at an alarming level for the year, although decreases are noted during the second half of the year.”

“The results from this report are evidence of the immense danger associated with drug abuse and more specifically prescription drug abuse,” said Jim McDonough, Director of the Florida Office of Drug Control. “Far too many Floridians are dying from prescription drugs. To address this problem Florida will continue to strengthen its efforts in the areas of prevention, treatment, and law enforcement in order to reduce the unacceptable amount of deaths that result from the abuse of prescription drugs.”

The number of HIV-positive drug users who inject has reached its highest level for more than a decade.

Official data from 2005 shows that one in 62 injecting drug users (1.6%) in England and Wales are HIV-positive. This compares with one in 110 in 2002.

Last year the number of HIV diagnoses among injecting drug users rose and rates among new users are also up.

The Health Protection Agency said the rise was partly due to an increase in the numbers injecting crack cocaine.

The level of HIV infection among injecting drug users remained stable in London but saw a six-fold increase in areas outside the English capital from one in 500 (or 0.2%) in 2002 to one in 83 (1.2%) in 2005.
Source: BBC News 17th March 2006

DRUG misuse is leading more young people than ever before to show up at hospital A&E departments with chest pain.

While chest pain is perceived as being associated with older generations, the increase in heroin and cocaine abuse is becoming more and more evident in hospitals as large numbers of young people present with symptoms mimicking heart related illnesses as a direct consequence of drug misuse.

“We are seeing a big increase in the abuse of cocaine and heroin and we are now also seeing it show up in our hospitals,” said Tony Barden, regional drugs co-ordination with the HSE South East.

“Young people are now coming in with chest pains association with drug misuse. This is an indication of heart and lung damage but we are just in our infancy where damage is concerned. The picture of just how serious the problem is will become a lot clearer over the next 18 months or so.”

Tony Barden says that serious health problems associated with cocaine and heroin abuse will only get worse and lead to more heart and lung complaints among those who use drugs.

“A lot of people are going out and having seven or eight, even 10 pints, and then mixing it with cocaine,” he said. “We need to be moving towards a scenario where we are working on testing for drugs as well as alcohol among motorists.”

The recently published Drugs Misuse Report 2005 showed that while the numbers coming forward for alcohol abuse treatment had dipped, there had been a marked increase in those seeking help for heroin and cocaine.

Data from the Liaison Officer at WRH, contained in the report, showed that 409 people admitted to the hospital after collapsing, hurting themselves or suffering serious ill-health, were then referred onto addiction services.
Source: Waterford News & Star 2nd June 2006

How likely you are to becoming a cocaine addict could well depend on your genetic make up, say researchers from the Institute of Psychiatry. Some people have a gene variation which stops the production of a protein that regulates dopamine in the brain.

The researchers said that if you have two copies of this gene variation, your chances of becoming addicted to cocaine are 50% higher.

You can read about this study in the Proceedings of the National Academy of Sciences. The study was funded by the Medical Research Council (UK).

The researchers studied the DNA of 1550 people. 700 of them were cocaine abusers while 850 were not.

We all produce a protein called DAT. DAT controls the removel of excess dopamine from the brain. Cocaine inhibits the action of DAT leading to dopamine overload. The dopamine overload is what gives the cocaine abuser the “high” feeling.

Part of our genetic code controls the production of DAT. The researchers found that people who had two copies of the variant that controls DAT production were 50% more likely to become cocaine addicts.

Obviously, if you have two copies of this variant and never touch cocaine your chances of becoming addicted to it are zero. Everyone will eventually become addicted to cocaine, if they take it often enough and for long enough. People with this gene variant are more likely to become addicted sooner.

Dr Gerome Breen, head researcher, said “This study is the first large scale search for a genetic variant influencing the risk of developing cocaine addiction or dependence. The target we investigated, DAT, is the single most important in the development of cocaine dependence. It made sense that variation within the gene encoding DAT would influence cocaine dependence.”

It was found that people who had the genetic variant were more likely to inhibit the DAT response when taking cocaine.

Hopefully, this new finding may eventually help in the designing of new drugs for the treatment of cocaine addiction, say the researchers.

“Drug abuse treatment can have important positive public health benefits even if the outcomes are less than perfect,” lead study author DL George Woody told Reuters Health. “The 12-step oriented combination of group and individual counselling worked the best, though all patients reduced their risk.”

Woody urged everyone to “support substance abuse treatment. It can do a lot of good both in the short and long term.”

In an article in the Journal of Acquired Immune Deficiency Syndromes, Dr. Woody who is at the University of Pennsylvania in Philadelphia and his colleagues report on changes in HIV risk among 487 people undergoing treatment for cocaine addiction.

Treatment was associated with an average reduction of cocaine use from 11 days per month to one day per month after six months, the authors report, with participants who received both individual and group drug counselling faring best.

Treatment participation was also associated with significant reductions in risky sex and the total risk of HIV infection, the report indicates.

Those who completed treatment showed a trend toward less sex risk and significantly less total risk than did patients who dropped out before completing their program, the researchers note.

HIV risk reduction corresponded to reductions in drug use and to improvements in psychiatric symptoms, the results indicate. This improvement was similar regardless of race, gender, sexual orientation or the presence of antisocial personality disorder.

“The fact that all treatments consisted of no more than three weekly outpatient sessions that included risk reduction counselling is worth noting,” the authors conclude, “because it suggests that reductions in cocaine use and HIV risk can be achieved at a relatively low cost, at least for a portion of the patients who seek treatment for cocaine dependence.”

A fifth of young adults whose blood vessels ruptured inside their brain abused drugs and more than 40% had malformed blood vessels, according to a study reported Feb. 17 at the American Stroke Association’s International Stroke Conference 2006 in Kissimmee, FL.

The study included 307 patients with intracerebral hemorrhage (ICH) — a stroke caused by a blood vessel bursting inside the brain. Of the 75 patients 49-years-old or younger, 20% had drugs in their system.

“The dominant drug of abuse was cocaine, long recognized as a risk factor for ICH,” said Michael Hoffmann, MD, lead author of the study and director of the stroke program at the University of South Florida-Tampa General Hospital. “Marijuana was another frequently abused drug and is beginning to emerge as a risk factor for stroke. Amphetamines also were commonly abused.”

How these drugs make brain blood vessels prone to rupture is not clear, but is being studied, Dr. Hoffmann said.

The study analyzed the causes and outcomes of ICH patients. 24% of ICH patients in a registry at Tampa General Hospital were ages 18 to 49. Half were women, about two thirds were Caucasian, 15% were black and 12% were Hispanic.

ICH is often linked with high blood pressure in people over age 50, and in this study, 57% of those age 50 and older had it. Only 33% of ICH patients ages 18 to 49 had high blood pressure.

Of the younger patients in the study, 41% had malformed blood vessels, known as arteriovenous malformations, aneurysms or other vascular disorders. Cerebral arteriovenous malformation occurs when blood vessels in the brain develop in an abnormal tangle in which the arteries connect directly to the veins without the normal capillaries between them. A cerebral aneurysm is the bulging of the wall of an artery in the brain. Both these conditions weaken blood vessels and increase the risk of a hemorrhagic (bleeding) stroke.

The good news is that patients under age 50 who experience this vessel rupture inside the brain have better outcomes than older patients.

“Surprisingly, our study showed a low mortality rate compared to population studies,” said Dr. Hoffmann, professor of neurology at USF.

The 30-day mortality was 14.6% for the younger group, significantly lower than for older patients, whose mortality rate was 21%, he said. Previously, national population studies have found a high 30-day mortality rate for stroke patients with ICH. Some epidemiological data have suggested a 45% to 50% mortality rate, Dr. Hoffmann said.

ICH has traditionally been associated with older age groups and higher mortality rates.

The younger patients came into the emergency room, then were rapidly transferred to a neurocritical care unit within six hours. Typically, patients are hospitalized in the neurocritical care unit for one to eight weeks. Patients were evaluated by MRI, CT and angiography.

“This new way of thinking about how to manage patients with ICH is an important approach, and patients are reaping benefits,” Dr. Hoffmann said.

Most of the younger patients were able to live independently three to six months after their ICH, with only mild to moderate cognitive impairment that tends to improve over time, he said.

Dr. Hoffmann said the degree and nature of disability at six months is now the focus of the extension of this study.

“Intensive neurocritical care is the key to successful outcome,” Dr. Hoffmann said. “Good medical care can salvage a high quality of life after a stroke.”

A fifth of young adults whose blood vessels ruptured inside their brain abused drugs and more than 40% had malformed blood vessels, according to a study reported Feb. 17 at the American Stroke Association’s International Stroke Conference 2006 in Kissimmee, FL.

The study included 307 patients with intracerebral hemorrhage (ICH) — a stroke caused by a blood vessel bursting inside the brain. Of the 75 patients 49-years-old or younger, 20% had drugs in their system.

“The dominant drug of abuse was cocaine, long recognized as a risk factor for ICH,” said Michael Hoffmann, MD, lead author of the study and director of the stroke program at the University of South Florida-Tampa General Hospital. “Marijuana was another frequently abused drug and is beginning to emerge as a risk factor for stroke. Amphetamines also were commonly abused.”

How these drugs make brain blood vessels prone to rupture is not clear, but is being studied, Dr. Hoffmann said.

The study analyzed the causes and outcomes of ICH patients. 24% of ICH patients in a registry at Tampa General Hospital were ages 18 to 49. Half were women, about two thirds were Caucasian, 15% were black and 12% were Hispanic.

ICH is often linked with high blood pressure in people over age 50, and in this study, 57% of those age 50 and older had it. Only 33% of ICH patients ages 18 to 49 had high blood pressure.

Of the younger patients in the study, 41% had malformed blood vessels, known as arteriovenous malformations, aneurysms or other vascular disorders. Cerebral arteriovenous malformation occurs when blood vessels in the brain develop in an abnormal tangle in which the arteries connect directly to the veins without the normal capillaries between them. A cerebral aneurysm is the bulging of the wall of an artery in the brain. Both these conditions weaken blood vessels and increase the risk of a hemorrhagic (bleeding) stroke.

The good news is that patients under age 50 who experience this vessel rupture inside the brain have better outcomes than older patients.

“Surprisingly, our study showed a low mortality rate compared to population studies,” said Dr. Hoffmann, professor of neurology at USF.

The 30-day mortality was 14.6% for the younger group, significantly lower than for older patients, whose mortality rate was 21%, he said. Previously, national population studies have found a high 30-day mortality rate for stroke patients with ICH. Some epidemiological data have suggested a 45% to 50% mortality rate, Dr. Hoffmann said.

ICH has traditionally been associated with older age groups and higher mortality rates.

The younger patients came into the emergency room, then were rapidly transferred to a neurocritical care unit within six hours. Typically, patients are hospitalized in the neurocritical care unit for one to eight weeks. Patients were evaluated by MRI, CT and angiography.

“This new way of thinking about how to manage patients with ICH is an important approach, and patients are reaping benefits,” Dr. Hoffmann said.

Most of the younger patients were able to live independently three to six months after their ICH, with only mild to moderate cognitive impairment that tends to improve over time, he said.

Dr. Hoffmann said the degree and nature of disability at six months is now the focus of the extension of this study.

“Intensive neurocritical care is the key to successful outcome,” Dr. Hoffmann said. “Good medical care can salvage a high quality of life after a stroke.”

According to the just released 46-nation Council of Europe annual report, both countries have a higher proportion of cocaine users than anywhere except Spain and Ireland tops the League’s Table for ecstasy. About 185 million people worldwide – 3% of the global population – use illegal drugs. Nearly 80% use cannabis, 20% use ecstasy and amphetamines, 7% use cocaine and 3% use heroin. The situation is now so bad that Europe is the most profitable market in the world for production and trafficking of drugs…
Source: The Scotsman, January 25, 2005.

Inbred strains of rats differ in how aggressively they seek cocaine after a few weeks of use, researchers say. The finding, posted online Jan. 18 by Psychopharmacology, is another piece of evidence that genetics plays a role in the relapse of drug-seeking behavior in humans, says Dr. Paul J. Kruzich, behavioral neuroscientist at the Medical College of Georgia and lead study author.

It also fingers glutamate, a neurotransmitter involved in learning and memory, as an accomplice in stirring the cravings and uncontrollable urges that drive some drug users to use again, he says.

“Given the right environmental stimuli, all persons addicted to psychostimulants can relapse, but potentially some people are a little more susceptible than others * it’s all about gene-environment interaction,” says Dr. Kruzich.

He took two strains of inbred rats – Fischer 344 and Lewis – with known genetic differences, enabled each to self-adminster cocaine for 14 days, then took the drug away for a week but not the levers the animals used to access it. During that hiatus, he adminstered a drug that stimulates glutamate receptors, possible targets for drugs of abuse.

He found that the F344 strain worked harder to get cocaine than the Lewis rats following treatment with the glutamate drug, suggesting they were more susceptible to relapse.

“Maybe 12-step programs and faith-based programs will be enough to keep some people from relapsing,” says Dr. Kruzich. “For others we may have to come up with medical treatments we can use on top of those to keep them from taking drugs again.”

He says there are many different versions of the hundreds of genes that may play a role in increasing the risk of relapse.

It’s known that some people become addicted more quickly than others, some literally with their first use, he says. The hardest part is not getting people to stop taking drugs: that happens when they are checked in a clinic or put in jail. The real work is keeping them from relapsing when they are out of such restricted environs, he says.

“Something happens, either they see an old colleague they have used with, they go into an old environment, they have a huge stressor in life and they start to want the drug. They have drug hunger, what we call drug craving,” says Dr. Kruzich. “When it gets bad enough, they engage in drug-seeking behavior.” His lab is working to identify the relapse trigger to use as a target for developing ways to curb craving and subsequent relapse.

His studies focus on an area of the brain called the nucleus accumbens core, a target for drugs of abuse long considered a pleasure center, Dr. Kruzich says. Drugs such as cocaine and methamphetamine stimulate release of dopamine in the nucleus accumbens. Dopamine is a neurotransmitter believed responsible for the euphoria that come with drug use. In fact, animals given dopamine blockers won’t self-adminster drugs of abuse, and dopamine has long been a focus of drug-abuse studies.

“These drugs impinge upon the reward centers of the brain that normally food, sex, survival and adaptation impinge upon,” says Dr. Kruzich. “When you are having that great piece of cheesecake and thinking, ‘Oh man,’ that is the kind of response these drug of abuse are evoking but much more so than that cheesecake could ever do.”

Glutamate, also released in the nucleus accumbens core, may play an equally important role in drug relapse, he says. Drugs such as cocaine appear to alter glutamate neurotransmission in the core, which may contribute to the rewiring of the brain that occurs with drug use. “It’s not that these drugs just damage neurons, which they can, but they rewire the circuitry of the brain so no longer is your spouse or your job or other things in your life important to you. Your brain is tricked into thinking that drugs are the most important thing for your survival,” Dr. Kruzich says.

Unfortunately, drugs that restore glutamate function also produce seizures, so scientists are looking for an indirect approach to restore the misdirected rewiring.

LONDON (Reuters) – Cocaine can cause serious abdominal problems as well as chest pain and breathing difficulties, a leading surgeon said on Friday.

“Abdominal complications from cocaine abuse are life-threatening and require emergency surgery,” said Luke Meleagros, of North Middlesex University Hospital, in Britain’s Journal of the Royal Society of Medicine.

With an estimated 344,000 people using cocaine and 17,000 taking crack cocaine each month in Britain, Meleagros and his colleagues fear health problems in drug users will increase, particularly in London where drug abuse is more common.

“As the number of cocaine abusers rises, we expect the accompanying health problems to spread across the country,” Meleagros said in a statement.

Cocaine is an addictive stimulant drug. Crack is a form of cocaine that comes in a rock crystal. The name derives from the crackling sound it produces when heated.

The drug can increase heart rate and blood pressure, as well as constrict blood vessels. Many cocaine-related deaths result from cardiac arrest or seizure.

“Abdominal complications are more common with users of crack cocaine and in poor, inner city areas,” said Meleagros.

“However, we suspect that there is an under-reporting or misrecognition of the problem in other areas, particularly affluent areas, as these complications occur in cocaine users as well.”

Symptoms of abdominal problems, which can occur within an hour of taking the drug, include pain, tenderness, nausea, vomiting and bloody diarrhoea.

Source: February issue (Vol. 99) of the Journal of the Royal Society of Medicine.

Inbred strains of rats differ in how aggressively they seek cocaine after a few weeks of use, researchers say.

The finding, posted online Jan. 18 by Psychopharmacology, is another piece of evidence that genetics plays a role in the relapse of drug-seeking behavior in humans, says Dr. Paul J. Kruzich, behavioural neuroscientist at the Medical College of Georgia and lead study author.

It also fingers glutamate, a neurotransmitter involved in learning and memory, as an accomplice in stirring the cravings and uncontrollable urges that drive some drug users to use again, he says.

“Given the right environmental stimuli, all persons addicted to psychostimulants can relapse, but potentially some people are a little more susceptible than others … it’s all about gene-environment interaction,” says Dr. Kruzich.

He took two strains of inbred rats – Fischer 344 and Lewis – with known genetic differences, enabled each to self-adminster cocaine for 14 days, then took the drug away for a week but not the levers the animals used to access it.

During that hiatus, he adminstered a drug that stimulates glutamate receptors, possible targets for drugs of abuse.

He found that the F344 strain worked harder to get cocaine than the Lewis rats following treatment with the glutamate drug, suggesting they were more susceptible to relapse.

“Maybe 12-step programs and faith-based programs will be enough to keep some people from relapsing,” says Dr. Kruzich. “For others we may have to come up with medical treatments we can use on top of those to keep them from taking drugs again.”

He says there are many different versions of the hundreds of genes that may play a role in increasing the risk of relapse.

It’s known that some people become addicted more quickly than others, some literally with their first use, he says. The hardest part is not getting people to stop taking drugs: that happens when they are checked in a clinic or put in jail. The real work is keeping them from relapsing when they are out of such restricted environs, he says.

“Something happens, either they see an old colleague they have used with, they go into an old environment, they have a huge stressor in life and they start to want the drug. They have drug hunger, what we call drug craving,” says Dr. Kruzich. “When it gets bad enough, they engage in drug-seeking behavior.”

His lab is working to identify the relapse trigger to use as a target for developing ways to curb craving and subsequent relapse.

His studies focus on an area of the brain called the nucleus accumbens core, a target for drugs of abuse long considered a pleasure center, Dr. Kruzich says. Drugs such as cocaine and methamphetamine stimulate release of dopamine in the nucleus accumbens. Dopamine is a neurotransmitter believed responsible for the euphoria that come with drug use. In fact, animals given dopamine blockers won’t self-adminster drugs of abuse, and dopamine has long been a focus of drug-abuse studies.

“These drugs impinge upon the reward centers of the brain that normally food, sex, survival and adaptation impinge upon,” says Dr. Kruzich. “When you are having that great piece of cheesecake and thinking, ‘Oh man,’ that is the kind of response these drugs of abuse are evoking but much more so than that cheesecake could ever do.”

Glutamate, also released in the nucleus accumbens core, may play an equally important role in drug relapse, he says. Drugs such as cocaine appear to alter glutamate neurotransmission in the core, which may contribute to the rewiring of the brain that occurs with drug use. “It’s not that these drugs just damage neurons, which they can, but they rewire the circuitry of the brain so no longer is your spouse or your job or other things in your life important to you. Your brain is tricked into thinking that drugs are the most important thing for your survival,” Dr. Kruzich says.

On June 22, 1998, ‘Wired for Addiction’ was presented as part of NIDA’s Frontiers in Neuroscience seminar series. The theme of these presentations centered on the neuronal remodeling that emerges after repeated substance use and withdrawal, with particular emphasis on the possibility of altered cognitive function as a consequence of the neural remodeling. Presentations were made by Drs. Ann Graybiel, Tony Grace, John Marshall, Janet
Neisewander, and Regina Carelli, and a summary and discussion was presented by Dr. Steve Grant of NIDA. Brief summaries of two presentations follow.

Chronic exposure to psychomotor stimulants may rewire your brain
Exposure to amphetamine and cocaine induces gene expression in cortico-basal ganglia circuits. Chronic intermittent exposure to the same drugs down-regulates some of the inducible change. After a course of chronic intermittent treatment and withdrawal of the drug, a subsequent challenge with the drug induces new patterns of gene expression in cortico-basal ganglia circuits. The repeated administration and withdrawal of cocaine induces both immediate early gene (lEG) expression after drug challenge in neurons that are not activated acutely, and an increase in the size of the area in which this response in observed. These findings raise the possibility that prolonged exposure to psychomotor stimulants produces enduring changes in brain wiring.

Ann Graybiel, Ph.D., Massachusetts Institute of Technology:

Neuronal interactions within the limbic system of rats: Alteration during amphetamine sensitization
Amphetamine exerts differential actions on neurons in the nucleus accumbens when given acutely versus repeatedly. The studies show that repeated amphetamine administration causes an increase in electrical coupling among nucleus accumbens neurons, which appears to be driven by an increase in prefrontal corticoaccumbens afferent activation. It is proposed that such a condition would lead to alteration of information flow within this system, resulting in a perseverance of behavioral action that may contribute to drug-seeking behavior in humans.

Imaging studies in humans suggest that the amygdala plays an important role in craving elicited by cocaine and cocaine-conditioned environmental stimuli. The research examined the relationship between neurochemical changes in the amygdala and cocaine-seeking behavior following exposure to a cocaine-paired environment or a cocaine priming injection. It measured cocaine-seeking behavior by assessing the persistence of lever-pressing in the absence of cocaine reinforcement in animals previously trained to press a lever for cocaine infusions. Lever-pressing under these conditions is thought to reflect the incentive motivational properties of cocaine and cocaine-associated stimuli. It first investigated whether the pattern of changes in cocaine-seeking behavior corresponded with changes in concentrations of dopamine in dialysates obtained from the amygdala during the course of cocaine withdrawal.

There were concomitant changes in cocaine-seeking behavior and dialysate dopamine following the cocaine priming injection, but not following exposure alone to the cocaine self-administration environment. It next investigated changes in Fos protein expression as a general marker for neuronal activation. Exposure to the cocaine self-administration environment, but not the cocaine priming injection, elicited Fos expression in the basolateral nucleus of the amygdala, nucleus accumbens shell, and cingulate cortex. In contrast, the cocaine priming injection, but not the environmental stimuli, elicited Fos expression in the central nucleus of the amygdala and dorsolateral caudate-putamen.

The findings suggest that different neural mechanisms mediate cocaine-seeking behavior elicited by cocaine conditioned environmental stimuli and those elicited by a priming injection of cocaine. Increases in extracellular dopamine may be critical for the induction of cocaine-seeking behavior elicited by cocaine but may not be elicited by cocaine-conditioned environmental stimuli.

This edition of Prevention Works lists some studies, which look at the gateway/addiction theory of progressive drug misuse. The implications for prevention are clear – Early use of nicotine, alcohol and marijuana is a predictor of later use of cocaine (etc. …)

Predicting continued use of marijuana among adolescents: the relative influence of drug-specific and social context factors.

Compared with people who used only one gateway drug (tobacco, alcohol and marijuana), children who used all three are 77 times more likely to use cocaine.
Children who smoke daily are 13 times more likely to use heroin than children who smoke less often.

Children who use marijuana are 85 times more likely to use cocaine than non-marijuana users. 90% of children who used marijuana, smoked or drank first. Children who drink are 50 times more likely to use cocaine than non drinkers.

Children who use gateway drugs – tobacco, alcohol and marijuana are up to 266 times more likely to use cocaine than those who don’t use any gateway drugs.
Study concludes nearly 90% of cocaine users smoked, drank and used marijuana

Center on Addiction and Substance Abuse at Columbia University (CASA), Oct. 27, 1994.

A 12- year-old who smokes is 30 times more likely to have used illicit drugs than a child of the same age who doesn’t smoke. This analysis proves that, for too many children cigarettes are a drug of entry into the world of illicit drugs

Center on Addiction and Substance Abuse at Columbia University (CASA), March 10, 1994.

Marijuana’s role as a gateway drug to serious drug use appears to have increased.

Abstract: Research has shown that adolescent users of tobacco are much more likely to progress to use of illicit drugs than are nonusers of tobacco. This article suggests potential psychosocial reasons for the progression based on principles of Learning Theory, Theory of Reasoned Action, Health Belief Model, and Cognitive Dissonance. In addition, a neuropharmacologic causal mechanism is discussed. The existence of tobacco’s gateway function has important implications in (the nation’s) efforts to reduce illicit drug use and adolescent smoking.

Gateway drugs — drugs of entry — serve as stepping stones to illicit drug use. Tobacco use in particular has proved a strong and consistent predictor of subsequent illegal drug use. Not all adolescent cigarette smokers progress to using marijuana or cocaine, but a strong statistical link exists between tobacco use and progression to illegal drugs. Research indicates it is incredibly rare for a “hard core” drug user to bypass the initial behaviour of cigarette use prior to using illicit drugs. Nicotine has been described as an “almost essential precursor” and a “necessary intermediate” to the use of marijuana and other drugs. Studies documented the link between adolescent smoking and illegal drug use. These studies indicate tobacco use consistently precedes illicit drug use, and the association shows a clear dose response pattern. The more adolescents smoke, the more likely they are to use illegal drugs. The statistical link between adolescent smoking and subsequent illegal drug use has been described by researchers as a “striking quantitative relationship” and a “dramatic association”. The contrast particularly becomes impressive when illegal drug use prevalence rates of adolescent daily cigarette smokers are compared to nonsmokers. Results vary, depending on which illegal drug is being studied, frequency of use (daily, monthly, ever) and the grades included in the study. One study showed the relative risk for illicit drug use among one pack or more daily teen smokers consistently at 10 to 30 times greater than for nonsmokers. Surveys by the U.S. Dept. of Health and Human Services demonstrated that young daily smokers were 114 times more likely to have used marijuana than those who had not smoked. Much of the statistical link between smoking and illegal drug use results from an indirect association where both behaviours share a common etiology caused by other psychosocial and environmental factors. However, an increasing number of researchers suggest the link between adolescent smoking and subsequent illicit drug use also results from causal mechanisms. While studies document a statistical association between the two behaviours, few propose theoretical models to explain potential causal mechanisms for the association. Yet, several potential psychosocial and neuropharmacologic causal mechanisms promote tobacco’s gateway drug function.

Clubbers who take ecstasy are 25% more likely to have a mental health disorder, compared to the general population, a survey has found. The UK average is one in five. Its findings back up previous scientific concerns over a link between ecstasy and mental health problems.
Ecstasy users are also twice as likely to have seen a doctor about a mental health problem compared to the rest of the population. Half of them asked about depression, which scientists believe could be linked to use of the Class A drug. But one in 10 users believed that taking ecstasy had made their lives worse overall. Both ecstasy and cocaine have been linked with mental health problems such as paranoia, panic attacks and depression.

Widespread drug use
The extent of drug use amongst clubbers is graphically illustrated by the fact 97% of 1 000 people surveyed said they had tried both E and cannabis at least once. Eleven per cent have tried heroin.
Mixmag estimates 1.5m people take ecstasy every weekend. But it says consumption has dropped by 13% among regular users. Ecstasy use had resulted in unplanned sex for one in three, one in 100 of which resulted in pregnancies. Half said their performance at work had been affected because of the drug. But the survey also found clubbers had developed a novel way of ensuring Ecstasy got into their bloodstream as quickly as possible – by taking it as a suppository. One in 15 surveyed by Mixmag admitted they had taken the drug in this way, a 200% increase compared to last year. Inserting it into the rectum allows the body to absorb it more quickly because of the large number of blood vessels in the anus.

Cocaine
Cocaine use fell 4%, though 45% of those surveyed said they still took the drug on a regular basis. Almost a third of cocaine users reported suffering a nosebleed after snorting the drug. Drug use appeared to be linked closely with high levels of alcohol use. More than a third of men who responded to the survey spent more than four nights a week in the pub. All respondents were three-and-a-half times more likely to injure themselves on alcohol than on ecstasy. They were also two-and-a-half times more likely to end up in the local casualty department. The survey also showed one in three said they had been violent on alcohol, compared with one in 10 on ecstasy. Twice as many had driven on ecstasy than on alcohol but drink drivers had a higher accident rate.

Physicians should consider the possibility of cocaine use as a culprit when young adults are brought to emergency rooms for nontraumatic chest pains, according to researchers at the UT Southwestern Medical Center at Dallas. Chest pain is the most common complaint of cocaine users, and in 1999 cocaine use was cited in 30 percent of all drug-related emergency department visits. In a review article published in today’s issue of The New England Journal of Medicine, Drs. Richard Lange and L. David Hillis report on the cardiovascular complications associated with cocaine use and effective treatments. “Death from cocaine abuse is on the rise in the United States,” said Hillis, who is vice chairman of internal medicine. “Early identification and understanding of cocaine-related cardiovascular complications are essential to their proper management.”

Lange and Hillis suggest that emergency medical physicians consider cocaine use in young patients with conditions such as arrhythmias, heart attack, inflammation of the heart muscle or dilated cardiomyopathy, a heart defect characterized by increased thickness of the wall of the left ventricle.

In 1999 an estimated 25 million Americans admitted that they had used cocaine at least once; 3.7 million had used cocaine in the past year; and 1.5 million were current users. In addition, medical examiners report that cocaine is the most frequent cause of drug-related deaths. Both Lange and Hillis have published extensively and made novel observations regarding cocaine-related heart disease.

In 1990 the researchers reported that beta-blockers, which are commonly administered to patients with chest pain, were not only ineffective but also detrimental in patients with cocaine-related chest pain. In a 1991 study Hillis and Lange reported that nitroglycerin, which dilates and relaxes blood vessels, had a beneficial effect on patients with cocaine-related chest pains. In 1994 the researchers found that verapamil hydrochloride, a calcium blocker, alleviated cocaine-induced constricted blood vessels. ‘Most cocaine-related chest pains are due to the fact that the blood vessels have been constricted,’ Hillis said. “The most effective treatment for this is nitroglycerin or calcium blockers.”

Source: Authors Dr. Richard Lange and L. David Hillis, published in The New England Journal of Medicine

Cocaine use among young adults in Britain is expanding faster than anywhere else in Europe according to a new Drug misuse report. The annual report from the Lisbon based European Monitoring Centre for Drugs and Drug Addiction, giving figures for 2000, shows that 5% of people in England and Wales between the ages of 16 and 29 took the drug at some point during the previous 12 months compared with 1% in 1996.

“Overall, the drug situation in the United Kingdom is very stable, but we have seen a sharp increase in the use of cocaine as it becomes more acceptable on the recreational scene, said Mike Trace, the United Kingdom’s former deputy drugs ‘tsar’ who now chairs the centres management board. Throughout Europe cannabis remains the most popular illegal drug. While 30% of British adults and 25% of Danes have smoked a cannabis cigarette at some point in their lives, just 10% of Finns have done so.

Source: The 2002 Annual Report on the State of the Drugs Problem in the European Union and Norway Reported in BMJ 2002; 325:794

Addiction specialists at Harvard University think they have found one reason that cocaine users seem to get sick so often; The drug restricts production of a body protein that triggers immune responses. Doctors have often noted that cocaine users suffer more infections, including the AIDS virus. One theory holds that this is because cocaine users are more likely to engage in dangerous behaviour such as unsafe sex. But a study published in this months Journal of Clinical Endocrinology and Metabolism suggests that cocaine also has a direct effect on the body’s infection-fighting chemistry. The study is one of a handful in the U.S. in which doctors injected human volunteers, rather than rats, with cocaine.

Researchers have now discovered another danger of cocaine use. For the first time, scientists have found cocaine significantly accelerates HIV infection. After infecting mice with the HIV virus, UCLA researchers injected half with liquid cocaine daily, while the other half received a placebo injection. Researchers counted the HIV-infected cells after 10 days and found a 200-fold increase in AIDS viral load in mice injected with cocaine compared to those that did not receive the drug. Gayle Baldwin, MD., from the UCLA AIDS Institute, says, ‘In only two weeks, the drug radically stimulated the production and spread of HIV.” In addition, mice with cocaine in their system had more than double the number of HIV-infected cells than cocaine-free mice.

Another significant finding shows a nine-fold decrease in immune cells in the cocaine-exposed mice. Dr. Baldwin says the drug increased HIV’s efficiency so much it nearly destroyed the immune cells HIV targets to destroy the immune system. She says, “Not only did the drug double the number of HIV-infected cells, it produced a nine-fold plunge in the number of T-cells that fight off the virus.” Researchers believe the animal study could lead to additional studies to examine the effects of diet, alcohol and other drugs on the spread of HIV infection.

Effects of cocaine on the coronary arteries
A study published in the American Heart Journal, commences with the following statement: “A number of studies have documented myocardial ischemia and infarction associated with cocaine use.” The authors did not think that a recreational dose of cocaine, though it increased heart rate by 30 beats and blood pressure by 20/10 mm hg, was significant enough to cause the well-documented sudden cardiac arrest associated with even small doses of cocaine. They noted that Cardiovascular toxicity is broad (cocaine use) ranging from acute aortic dissection or rupture to stoke. Important cardiac complications include sudden death, acute reversible myocarditis, dilated cardiomyopathy, life-threatening arrhythniias, and myocardial ischemia and infarction’. The study found that cocaine causes the diameter of the coronary artery to constrict while at the same time increasing the heart’s need for oxygen. Additionally, they found that cocaine creates a milieu that is favourable to thrombosis (blood clotting). Their conclusion was that these effects, coupled with changes in blood platelets, all worked together to contribute to cardio-vascular problems associated with cocaine use.

Cocaine toxic effect on endothelium-dependent vasorelaxation: an in vitro study on rabbit aorta
This study examined the toxic effect of cocaine on the vascular system of rabbit hearts. The authors commented that “These findings contribute to clarifying the toxicological profile of cocaine on the vascular target, providing a further explanation for cocaine’s capacity to induce vascular disorders.”

Cocaine induced hypokalaemic periodic paralysis
A recent report in a medical journal discusses ‘episodes of paralysis after engaging in a cocaine binge,’ and states that the use of cocaine has been associated with a number of psychiatric, medical and neurological complications.

Epidemic Crack Cocaine Use Linked with Epidemics of Genital Ulcer Disease and Heterosexual HIV Infection in the Bahamas
A crack cocaine epidemic in the Bahamas, which began in 1982, was found to be the primary factory leading to an epidemic of Genital Ulcer Disease (GUD) and heterosexual HIV infection in that country. By 1999 the Bahamas had the highest rate of reported AIDS in the northern hemisphere. The authors wrote: “The important role of crack cocaine use in facilitating transmission of STD… among inner-city populations in the United States has been repeatedly described. Several studies have shown the risk behaviours associated with use of cocaine, and an increased risk of transmission has been demonstrated to be a consequences of trading sex for drugs. The phenomenon of crack cocaine-enhanced transmission of STD, including HIV infection, has not yet been extensively documented outside North America and the Caribbean. Nonetheless, recognition of this association in North America has alerted other countries to be vigilant in avoiding the crack cocaine epidemic.”

Source: Author Gomez et al, Sexually Transmitted Diseases – May 2002

Cocaine Use, Hypertension, and End-State Renal Disease
A number of recent studies have noted a correlation between kidney failure (end-stage renal disease – ESRD), high blood pressure (hypertension – HTN) and the use of cocaine. In the U.S., Medicare, funded by federal tax dollars, covers the cost of dialysis and transplantation. This study evaluated 193 black patients from two urban hemodialysis units. The authors noted that “Cocaine use among blacks has increased nearly 100% since 1985, now accounting for approximately 23% of U.S. cocaine use. Cocaine use has been linked to HTN, cardiac and cerebrovascular events and acute renal failure, but only recently to chronic renal failure. 113 of the subjects had HTN-ESRD and of those 49 had used cocaine, either alone or in combination with other drugs.

The operator of the Baltimore Light Rail train that ploughed into a steel barrier at Baltimore Washington International Airport on Feb 13, injuring 22 passengers, tested positive for cocaine after the crash, transportation officials said yesterday: Sam Epps, who had worked for the Maryland Mass Transit Administration for 25-years, was fired Feb 17. He told investigators he was under the influence of prescription drugs at the time of the crash, MTA officials said. The next day, agency officials said, they received the drug test results that showed Epps was under the influence of cocaine.

Researchers determined that women who use cocaine during pregnancy risk affecting the brain structure of their children. In studying the brains of rhesus monkeys, researchers at the University of Maryland found that prenatal cocaine use could result in the loss of more than half of the brain cells in the infant’s cerebral cortex. The highest level of the brain, the cerebral cortex is responsible for such functions as sensation, voluntary muscle movement, thought, reasoning, and memory.

“This is the first study that clearly shows the possibility that cocaine may affect the brain structure. It shows that it could happen,” said Dr. Michael Lidow, one of the study’s authors. “This is a warning sign. For the study, four monkeys were born to mothers who were given 20mg/kg of cocaine per day during the second trimester of pregnancy. Four other monkeys received no cocaine. Researchers found that that the cerebral cortex in the monkeys whose mothers received cocaine contained 60 percent fewer neurons and was about 20 percent smaller than that of the monkeys who received no cocaine.

Lidow said additional research is needed to determine how the study’s findings may apply to humans.

Source: Author Dr. M. Lidow. Published in the Journal of Comparative Neurology. June 2001

More teenagers are using cocaine and regularly smoking and drinking, but an increasing number are also wearing seat belts and refusing to ride with a driver who’s been drinking. Those results were released yesterday in a survey conducted by the Centres for Disease Control and Prevention.

The survey examined the behaviour of 13 600 high school students across the country. The survey found injury and violence-related behaviours have fallen, but lads still regularly smoke and drink – nearly half said they’d consumed more than one alcoholic beverage more than once in the month before the survey.

Using cocaine, in particular crack cocaine, can result in a fatal tear in the major blood vessel leaving the heart. While cases of aortic dissection are rare, Dr. Priscilla Y. Hsue of the University of California at San Francisco said researchers at San Francisco General Hospital found an unusually high incidence of the condition among cocaine users.

In reviewing all cases of aortic dissection at the hospital over the past 20 years, researchers found that 14 of the 38 cases were directly related to cocaine use. All but one patient had used the drug in the form of crack cocaine. The condition is fatal unless the patient receives prompt emergency surgery. Hsue recommended that doctors and nurses be aware of aortic dissection in cocaine users with chest pain.

Cocaine damages or even kills the very brain cells that trigger the “high” felt by users of the drug, scientists said today. This first direct evidence of cocaine-induced damage to key cells in the brain’s “pleasure centre” could help explain many aspects of cocaine addiction. It might also aid the development of new anti-addiction drugs and increase understanding of other disorders involving the same brain cells, such as depression.

The American study was performed at the University of Michigan Health System and the VA Ann Arbor Healthcare System. Leader researcher Karley Little said: “This is the clearest evidence to date that the specific neurons cocaine interacts with don’t like it and are disturbed by the drug’s effects”. The study involved post-mortem brain tissue samples from cocaine abusers and control subjects. The samples were from 36 known cocaine abusers and 35 non-drug users of similar age, sex, race and causes of death. The team looked at the cells of the brain that release a pleasure-signalling chemical called dopamine. They analysed overall dopamine levels as well as the amount of a protein called VMAT2 which interacts with dopamine.

The researchers found levels of dopamine and the VMAT2 protein were significantly lower in cocaine users than control subjects. They also found levels tended to be lowest in cocaine users with depression. The research gives the strongest indication yet that dopamine neurons are harmed by cocaine use. Dopamine triggers the actions required to repeat previous pleasures and helps us work, feel emotions and reproduce. It is also involved in a drug users “high’ as cocaine causes levels to build up and so the pleasure signals are repeated over and over. Long-term effects of cocaine on the dopamine system could contribute to addicts’ cravings and account for their decreased motivation, stunted emotions and uncomfortable withdrawal symptoms. Professor Little said the study highlighted the fragility of dopamine neurons and ‘the vicious cycle that cocaine use can create’.

Source: Author Professor K. Little et al. Published in the American Journal of Psychiatry, Jan 2003

Cocaine use “is even more dangerous than we had previously known”. Cocaine causes blood to thicken by increasing the number of red blood cells, and by triggering an increase in a protein that causes platelets to stick together. The ‘double whammy’ can cause clotting that can lead to heart attacks and strokes. A previous study, released in June, showed cocaine users are 24 times more likely to have a heart attack during the first hour after taking the drug. The new study may help explain why.

This study measured changes in the blood of 21 people for an hour after they sniffed a moderate amount of cocaine, or received it intravenously. Red blood cell counts increased 4-6% on average after individuals ingested the drug, due to constriction of the spleen. Cocaine causes the constricting by pumping more red blood cells into the system, Siegel said. The thickened blood must circulate through already-constricted vessels, creating a potentially dangerous situation, Siegel said. Previous studies have shown that cocaine use causes blood vessels to narrow. The study suggests that anticoagulants may be useful in treating cocaine-induced chest pains, Siegel said. He said it provides further warning to athletes who might use cocaine, or substances with a similar effect, in an attempt to enhance performance. While the study’s small sample size made the conclusions preliminary, “we’re very confident that both of these observations are real, he said. The study also found an average 40% increase in a blood protein known as the von Willebrand factor in subjects who received cocaine intravenously. The von Willebrand factor promotes clotting by causing platelets to stick together.

Dr. Steve Frohwein, a cardiologist and assistant professor at the Emory University School of Medicine in Atlanta said several factors – such as infection, cancer or other toxins – can lead to clotting. “Cocaine just stimulates a well-known cascade of events,’ said Frohwein, who was not involved in the study.

Hemorrhagic strokes are significantly more likely to occur in recent cocaine users than in individuals who do not use cocaine, and the mortality rate is also significantly greater.

Dr. Anil Nanda and colleagues, from the Louisiana State University Health Sciences Center in Shreveport, compared stroke outcomes in 16 patients with positive toxicology tests for cocaine with outcomes in 38 patients who had not used cocaine, eight of the cocaine users (50%) had a hemorrhagic stroke compared with just one patient (3%) in the control group. The cocaine users were between 18 and 48 years of age, while the non using group was ‘slightly older,” Dr. Nanda said. Neurosurgical interventions for removal of the aneurysms were completed in all but one of the patients during the 6-year study. The researchers report satisfactory outcomes at 30 days post event in 83% of controls, while just 31% of cocaine users achieved a satisfactory outcome. The mortality rate was 56% for the cocaine users compared with just 2.7% in controls, Dr. Nanda said. The patient groups showed no significant difference in history of hypertension or smoking.
“We need to create a stronger awareness that cocaine does cause strokes”Source: Dr. Anil Nanda et al, Louisiana State University Shreveport, Reported in 68th annual meeting American Association of Neurological Surgeons California, April 2000

Cocaine may be one of the toughest addictions to cure because it triggers a build up of a protein that persists in the brain and stimulates genes that intensify the craving for the drug, new research suggests. Scientists at the Yale School of Medicine were able to isolate the long-lived protein, called Delta-FosB, and show that it triggered addiction when released to a specific area of the brains of genetically engineered mice. The protein (pronounced fawz-bee) isn’t produced in the brain until addicts have used cocaine several times, or even for several years. But once the build up begins, the need for the drug becomes overpowering and the user’s behaviour becomes increasingly compulsive.
“It’s almost like a molecular switch,” said Eric Nestler, who led the research. ‘Once it’s flipped on, it stays on, and doesn’t go away easily.” The findings were called “elegant” and “brilliant’ by other researchers who said it offered the first concrete proof that drug use triggers a specific long-term change in brain chemistry.

Nestler and his colleagues combined genetic and biochemical research to isolate the Delta-FosB protein and the area of the brain it affected, then did behavioural studies on the mice. Once the level of Delta-FosB accumulates, it begins to regulate genes that control a region of the brain called the nucleus accumbens. an area involved in addictive behaviour and pleasure responses. They speculated that Delta-FosB also activates other genes that produce biochemical compounds called glutamates, which carry messages in brain cells. Receptors in the brain cells become highly sensitive to glutamate, particularly in the nucleus accumbens. To test the theory, they inserted a gene associated with glutamate into the nucleus accumbens of experimental mice. Those mice showed a ‘dramatic increase in cocaine sensitivity, they reported. “This is a major advance in our understanding of addiction,’ said Francis White, chairman of cellular and molecular pharmacology at Finch University of Health Sciences in Chicago.

Other researchers were more cautious, noting that addiction is a complex process in humans because it is linked to learning and multiple chemical pathways in the brain. “It’s not clear to me that there’s a separate molecular pathway that’s going to be assignable to drug abuse and not interfere with other learning,’ said Gary Aston-Jones of the University of Pennsylvania School of Medicine. The craving for cocaine can be so powerful, a recovered addict who has avoided the drug for years may start feeling his or her heart race just by seeing something associated with drug use, such as a $100 bill or a familiar street corner, Aston-Jones said. “You want to knock out the memory for the drug but you don’t want to knock out the memory for the way home,” he said. Steve Hyman, director of the National Institute of Mental Health, said the study also indicated the build up of the Delta-FosB protein might be a factor with other drugs, including amphetamine, morphine, heroin and nicotine.

Researchers found that repeated exposure to cocaine causes a genetic change that leads to altered levels of a specific brain protein called cyclin-dependent kinase 5 (Cdk5). Previous research found that Cdk5 regulates the action of dopamine, a chemical messenger in the brain associated with cocaine’s pleasurable ‘rush’ and with addiction to cocaine and other drugs. Scientists discovered that delta-FosB, a protein, triggers increases in Cdk5 levels. These results suggest that delta-FosB-mediated changes in Cdk5 levels and the resulting alterations in dopamine signalling in brain cells contribute to adaptive changes in the brain related to cocaine addiction,’ said Dr. James Bibb of Rockefeller University in New York City, N.Y., who was involved in the study.

“This research provides a valuable insight into the step-by-step molecular adaptations that the brain makes in response to drugs,” said Dr. Alan I. Leshner, director of NIDA. “These adaptations result in long-term changes at the cellular level that are involved in the development of addiction.”

Source: Dr James Bibb et al Rockefeller University New York city published in Nature March 2001

The huge number of Jamaican women coming into Britain with their stomachs full of cocaine is pushing the already overcrowded female prison system to breaking point. More than 10% of the women currently in prison. Jamaican drug mules who swallowed rubber wraps of cocaine and boarded flights to this country. A Guardian investigation has established that the long sentences being served by the 450 Jamaican couriers are stretching resources to the limit while failing to act as a deterrent to the desperate women prepared smuggle drugs. The crisis has deepened since July, when a glut of women prisoners were sentenced before the courts summer recess. Women are regularly being moved around as prisons try to find them cells and overcrowding blamed for the unprecedented number of suicides within female jails: 17 women have taken their own life since August last year.Source: Guardian.co.uk Oct 2003

Apart from having mood elevating properties, cocaine is capable of causing myocardial infarction, arrhythmia, sudden death, stroke, seizures, bowel necrosis, and numerous other complications… the full extent of the effects of cocaine on the kidney, however, has become apparent more recently. Additionally, van der Woude noted: “A retrospective study has suggested that cocaine exposure in utero leads to an increased incidence of hypospadia and an increased incidence of renal (kidney) tract abnormalities.

After years of dismissing cocaine as a U.S. problem, Mexicans are finding that its their problem too. Government drug treatment clinics that saw 3 000 abusers a year in the 1990s now see 50 000 a year. Abuse used to be largely confined to the northern Mexican states from which U.S. cocaine smuggling operations were launched. Now it has spread south to larger cities such as Mexico City and Guadalajara.

Physicians should consider the possibility of cocaine use as a culprit when young adults are brought to emergency rooms for nontraumatic chest pains, according to researchers at the UT Southwestern Medical Center at Dallas. Chest pain is the most common complaint of cocaine users, and in 1999 cocaine use was cited in 30 percent of all drug-related emergency department visits. In a review article published in today’s issue of The New England Journal of Medicine, Drs. Richard Lange and L. David Hillis report on the cardiovascular complications associated with cocaine use and effective treatments. “Death from cocaine abuse is on the rise in the United States,” said Hillis, who is vice chairman of internal medicine. “Early identification and understanding of cocaine-related cardiovascular complications are essential to their proper management.”

Lange and Hillis suggest that emergency medical physicians consider cocaine use in young patients with conditions such as arrhythmias, heart attack, inflammation of the heart muscle or dilated cardiomyopathy, a heart defect characterized by increased thickness of the wall of the left ventricle.
In 1999 an estimated 25 million Americans admitted that they had used cocaine at least once; 3.7 million had used cocaine in the past year; and 1.5 million were current users. In addition, medical examiners report that cocaine is the most frequent cause of drug-related deaths. Both Lange and Hillis have published extensively and made novel observations regarding cocaine-related heart disease.
In 1990 the researchers reported that beta-blockers, which are commonly administered to patients with chest pain, were not only ineffective but also detrimental in patients with cocaine-related chest pain. In a 1991 study Hillis and Lange reported that nitroglycerin, which dilates and relaxes blood vessels, had a beneficial effect on patients with cocaine-related chest pains. In 1994 the researchers found that verapamil hydrochloride, a calcium blocker, alleviated cocaine-induced constricted blood vessels. ‘Most cocaine-related chest pains are due to the fact that the blood vessels have been constricted,’ Hillis said. “The most effective treatment for this is nitroglycerin or calcium blockers.”

Source: Authors Dr. Richard Lange and L. David Hillis, published in The New England Journal of Medicine.

Cocaine use among young adults in Britain is expanding faster than anywhere else in Europe, according to a new Drug misuse report. The annual report from the Lisbon based European Monitoring Centre for Drugs and Drug Addiction, giving figures for 2000, shows that 5% of people in England and Wales between the ages of 16 and 29 took the drug at some point during the previous 12 months compared with 1% in 1996.

“Overall, the drug situation in the United Kingdom is very stable, but we have seen a sharp increase in the use of cocaine as it becomes more acceptable on the recreational scene, said Mike Trace, the United Kingdom’s former deputy drugs ‘tsar’ who now chairs the centres management board. Throughout Europe cannabis remains the most popular illegal drug. While 30% of British adults and 25% of Danes have smoked a cannabis cigarette at some point in their lives, just 10% of Finns have done so.

Source: The 2002 Annual Report on the State of the Drugs Problem in the European Union and Norway Reported in BMJ 2002; 325:794.

Addiction specialists at Harvard University think they have found one reason that cocaine users seem to get sick so often; The drug restricts production of a body protein that triggers immune responses. Doctors have often noted that cocaine users suffer more infections, including the AIDS virus. One theory holds that this is because cocaine users are more likely to engage in dangerous behaviour such as unsafe sex. But a study published in this months Journal of Clinical Endocrinology and Metabolism suggests that cocaine also has a direct effect on the body’s infection-fighting chemistry. The study is one of a handful in the U.S. in which doctors injected human volunteers, rather than rats, with cocaine.

Researchers have now discovered another danger of cocaine use. For the first time, scientists have found cocaine significantly accelerates HIV infection. After infecting mice with the HIV virus, UCLA researchers injected half with liquid cocaine daily, while the other half received a placebo injection. Researchers counted the HIV-infected cells after 10 days and found a 200-fold increase in AIDS viral load in mice injected with cocaine compared to those that did not receive the drug. Gayle Baldwin, MD., from the UCLA AIDS Institute, says, ‘In only two weeks, the drug radically stimulated the production and spread of HIV.” In addition, mice with cocaine in their system had more than double the number of HIV-infected cells than cocaine-free mice.

Another significant finding shows a nine-fold decrease in immune cells in the cocaine-exposed mice. Dr. Baldwin says the drug increased HIV’s efficiency so much it nearly destroyed the immune cells HIV targets to destroy the immune system. She says, “Not only did the drug double the number of HIV-infected cells, it produced a nine-fold plunge in the number of T-cells that fight off the virus.” Researchers believe the animal study could lead to additional studies to examine the effects of diet, alcohol and other drugs on the spread of HIV infection.